PubMed Trending Research Digest — July 07, 2026

A curated digest of 100 trending PubMed articles, automatically categorised and summarised across 15 research areas.

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Immunotherapy & Cancer Clinical Trials (Checkpoint/Antibody/ADC/Combination) Targeted Protein Degradation (PROTACs) & Epigenetic Targets Cancer Cell Mechanisms & Therapeutic Resistance (Non-clinical) Nanomedicine & Drug Delivery (including EVs/exosomes/nanocarriers) Metabolic Disease, Insulin Resistance & Obesity (Mechanisms/Models) Diabetes & Cardiovascular Risk Prediction/Prognosis (Cohorts/Markers) Cardiovascular Disease Prevention & Real-world Comparative Effectiveness Aging, Biological Age & Longevity Biomarkers/Models Neurodegeneration & Neuroinflammation (Mechanisms/Targets) Neurodevelopmental Disorders & Genetics (ASD/Autism; rare variants) Neuromuscular & Muscle Regeneration (including exercise/rehab) Infectious Disease Epidemiology, Vaccines & Antimicrobials Host-Pathogen Immunity & Antiviral Mechanisms Autoimmunity, Inflammation & Immune Profiling (non-cancer) Reproductive/Endocrine & Women’s/Men’s Health Biomarkers

Automated digest · 100 articles · 15 research areas · July 07, 2026

Overview

Across this week’s set, a dominant theme is “systems-level” biology informing therapy: multi-omics and single-cell approaches are used to map immune or metabolic states (e.g., macrophage ER stress in diabetic wounds; immune-inflammatory trajectories in older adults with sepsis; glial programs in Parkinson’s; glial water-channel dysregulation early in TDP-43 models). These studies increasingly treat disease as dynamic—tracking how trajectories of biomarkers, immune profiles, or microbiome functions relate to outcomes such as regeneration, mortality, or neurocognitive decline.

A second major thread is targeted intervention that exploits specific molecular vulnerabilities. In oncology, the pipeline spans clinical testing of checkpoint/chemo combinations and targeted regimens (biliary tract cancer; diffuse large B-cell lymphoma; post–durvalumab strategies) alongside mechanistic work on resistance drivers (SEPTIN7–FGFR4 in HCC; MLKL–ESCRT-III ferroptosis resistance; KRASG12D-selective vulnerability; replication-stress biology via PARG inhibition). Parallel to this, protein-degradation platforms (STAT3 and BRD4 PROTACs) and next-generation ADC concepts highlight a shift toward higher-efficacy, mechanism-driven therapeutics.

Finally, several studies connect metabolism, inflammation, and neurobiology—often through delivery or signaling intermediates. EV/nanoparticle and gene-delivery platforms (EV-loaded hydrogels for diabetic wound repair; exosome capture for prostate cancer detection; non-viral astroglia-to-neuron reprogramming; AAV capsid selection for CNS delivery) illustrate how engineering is being used to translate mechanistic insights into practical interventions. Meanwhile, reviews and cohorts emphasize risk stratification beyond single measurements—using longitudinal mismatch patterns, TyG/anthropometric trajectories, proteomics for valvular disease, and insulin-resistance surrogates in MASLD/NAFLD—while aging frameworks (e.g., ORGAN-AGE) push the field toward more rigorous interpretation of “biological age” signals.

Immunotherapy & Cancer Clinical Trials (Checkpoint/Antibody/ADC/Combination)

Cisplatin-gemcitabine-durvalumab reintroduction in advanced biliary tract cancer: a multinational real-world analysis.

This multinational real-world cohort study evaluated reintroduction of cisplatin-gemcitabine-durvalumab (CGD) in patients with advanced biliary tract cancer (BTC) who progressed during durvalumab maintenance, comparing outcomes with FOLFOX/XELOX. CGD reintroduction was assessed for overall survival (OS) and progression-free survival (PFS) in the maintenance-progressing population, addressing whether platinum-based chemotherapy can restore disease control after prior chemoimmunotherapy. The clinical significance is that it informs treatment selection for advanced BTC after durvalumab maintenance failure, where effective post-progression options are limited.

Camera S, Vogel A, Rimini M et al. · ESMO open · (2026) · View on PubMed ↗

Polatuzumab Vedotin Plus Rituximab, Gemcitabine, and Oxaliplatin in Relapsed or Refractory Diffuse Large B-Cell Lymphoma: Results From the Phase III, Randomized POLARGO Trial.

In the phase III randomized POLARGO trial, investigators tested polatuzumab vedotin plus rituximab, gemcitabine, and oxaliplatin (Pola-R-GemOx) in transplant-ineligible relapsed or refractory diffuse large B-cell lymphoma (R/R DLBCL). The study reports efficacy and safety of this Pola-R-GemOx regimen as an alternative therapy for patients with poor prognosis after first-line failure. This is scientifically and clinically significant because it evaluates a targeted antibody-drug conjugate–based combination strategy in a defined DLBCL subgroup that cannot receive autologous stem cell transplant.

Matasar M, Li Z, Vassilakopoulos TP et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Next-Generation Checkpoint Combinations: Optimizing PD-(L)1-Based Therapy Across the Advanced, Adjuvant, and Neoadjuvant Settings.

This Current Oncology Reports review synthesizes evidence on “next-generation” combinations of PD-(L)1 inhibitors across advanced, adjuvant, and neoadjuvant settings, focusing on renal cell carcinoma (RCC), urothelial (bladder) cancer, and non-small cell lung cancer (NSCLC). It highlights how resistance to PD-(L)1 monotherapy drives the development and positioning of combination regimens and summarizes the most mature, practice-relevant combination strategies in these tumor types. The significance is that it provides a framework for optimizing PD-(L)1-based therapy sequencing and combination selection to improve durability of benefit.

Petrelli F, Colombo Zefinetti L, D’Alessio A et al. · Current oncology reports · (2026) · View on PubMed ↗

Carfilzomib, lenalidomide, and dexamethasone (KRd) versus bortezomib, lenalidomide, and dexamethasone (VRd) induction prior to autologous haematopoietic stem cell transplant/transplantation in newly diagnosed multiple myeloma.

This retrospective single-center study compared induction regimens—carfilzomib, lenalidomide, and dexamethasone (KRd) versus bortezomib, lenalidomide, and dexamethasone (VRd)—in newly diagnosed multiple myeloma patients undergoing upfront autologous hematopoietic stem cell transplantation. Patients receiving KRd more often had high-risk cytogenetics and higher R2-ISS stage, and the analysis assessed pretransplant response outcomes (e.g., complete response and very good partial response) between regimens. The clinical significance is that it provides comparative real-world evidence on induction strategy selection prior to transplant in NDMM, especially relevant for risk-stratified patients.

Marcoux C, Milton DR, Tanner MR et al. · British journal of haematology · (2026) · View on PubMed ↗

Orelabrutinib versus chemoimmunotherapy in treatment-naïve chronic lymphocytic leukemia/small lymphocytic lymphoma: a randomized, phase 3 trial.

This randomized phase 3 trial studied orelabrutinib, an irreversible and selective BTK inhibitor, versus chlorambucil plus rituximab in treatment-naïve chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) patients (NCT04578613; n=192). The abstract indicates the trial was designed to compare efficacy with progre[ssion]-related primary endpoint(s) at a median follow-up of 21.4 months, with patients randomized 1:1 to orelabrutinib (n=91) or chlorambucil+rituximab (n=101). If efficacy and safety favor orelabrutinib, this would support BTK-inhibitor–based first-line regimens as an alternative to chemoimmunotherapy for CLL/SLL.

Li F, Zhou K, Xu W et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Durvalumab with gemcitabine-based chemotherapy regimens in advanced biliary tract cancer: primary results from the phase IIIb TOURMALINE study.

In the phase IIIb TOURMALINE study (NCT05771480), researchers evaluated durvalumab plus gemcitabine-based chemotherapy regimens in a close-to-real-world first-line advanced biliary tract cancer population, including patients with poor prognosis. Participants received IV durvalumab 1500 mg with investigator-selected gemcitabine-based regimens, and the report provides primary results on safety and efficacy. This extends evidence for durvalumab–chemotherapy combinations beyond the original TOPAZ-1 trial into broader, more heterogeneous clinical practice settings.

Oh DY, Ikeda M, Macarulla T et al. · Journal of hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Advances in antibody-drug conjugates in cancer: latest updates from the 2026 AACR annual meeting.

This review summarized the latest advances in antibody-drug conjugates (ADCs) presented at the 2026 AACR Annual Meeting, focusing on new design strategies and therapeutic concepts. The key finding was that ADC development is moving toward dual/multi-payload constructs, multispecific targeting, and immunostimulatory payloads, including approaches aimed at the tumor microenvironment such as depletion of regulatory T cells and tumor-associated macrophages. These updates are significant because they address major ADC limitations—tumor heterogeneity, resistance, and systemic toxicity—by expanding targeting and payload functionality.

Li YR, Zhu Y, Chen Y · Experimental hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Targeted Protein Degradation (PROTACs) & Epigenetic Targets

Discovery of SD-2301 as a Highly Potent and Selective PROTAC STAT3 Degrader Capable of Achieving Complete Tumor Regression with Single Administration.

This study developed and characterized the PROTAC STAT3 degrader SD-2301 using high-affinity STAT3 ligands and Von Hippel–Lindau (VHL) E3 ligase recruitment, testing its activity in STAT3-dependent cancer cell models. SD-2301 achieved DC50 = 4 nM with >95% maximal STAT3 degradation, showed >100-fold improved potency over SD-36/SD-91, and induced strong growth inhibition (IC50 = 5–11 nM) in SU-DHL-1 and SUP-M2 lymphoma cells. These data indicate that SD-2301 can drive near-complete STAT3 degradation with single-administration tumor regression potential, supporting STAT3 PROTACs as a high-efficacy anticancer strategy.

Acharyya RK, Bai L, Zhou H et al. · Journal of medicinal chemistry · (2026) · View on PubMed ↗ · Free PDF ↗

GID4-Recruiting PROTACs for BRD4 Degradation Overcome Resistance Driven by CRBN and VHL Deficiency.

This study designed a GID4-recruiting PROTAC (compound a11) to degrade BRD4 by recruiting the CTLH E3 ligase substrate receptor GID4, and tested it in VHL- and CRBN-deficient cellular models. a11 induced GID4-dependent BRD4 degradation via the ubiquitin–proteasome pathway (DC50 = 0.21 ± 0.04 μM) and retained activity in VHL- and CRBN-deficient settings, including stronger antiproliferative effects in VHL-deficient 786-O renal cell carcinoma cells. These findings support GID4-recruiting PROTACs as a way to overcome resistance mechanisms caused by CRBN and VHL deficiency.

Tang Y, Zhang M, Fang Y et al. · Journal of medicinal chemistry · (2026) · View on PubMed ↗

Cancer Cell Mechanisms & Therapeutic Resistance (Non-clinical)

SEPTIN7 Enhances Tumorgenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling.

This Cancer Research study examined the role of the small GTPase SEPTIN7 in hepatocellular carcinoma (HCC) tumorigenesis and therapeutic resistance, using human HCC samples, HCC cell lines, and patient-derived organoids, and performing genetic knockout of Septin7 in hepatocytes. SEPTIN7 was upregulated in high-stemness human HCC and promoted cancer stem cell self-renewal and resistance to therapy, mechanistically by promoting FGFR4 stabilization and recycling. The findings are significant because they identify SEPTIN7 as a potential therapeutic target to overcome FGFR4-driven resistance and recurrence in HCC.

Sun T, Sun Q, Zhang X et al. · Cancer research · (2026) · View on PubMed ↗

Development and Validation of a Pathomics Model for Prognosis Prediction in Neoadjuvant Therapy-Treated Breast Cancer: A Retrospective, Multicenter Study.

This retrospective multicenter study developed and validated a multimodal AI pathomics model (ClinicHistomics Integrated Outcome Prediction Model, CIOPM) for prognosis prediction in neoadjuvant therapy-treated breast cancer patients. By integrating clinicopathological variables with hematoxylin-and-eosin (H&E) whole-slide images (WSIs) from 847 WSIs across four cohorts, it reports robust predictive performance in model development and external validation. The clinical significance is that CIOPM could support more personalized prognostication after neoadjuvant therapy using routine pathology data.

Wei Y, Lou W, Han Z et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

Osimertinib Resistance in EGFR-Mutated Non-Small Cell Lung Cancer: Mechanisms and Therapeutic Strategies.

This review focused on mechanisms of acquired resistance to osimertinib, a third-generation EGFR tyrosine kinase inhibitor, in EGFR-mutated non-small cell lung cancer (NSCLC). It summarizes key resistance pathways, including EGFR-dependent and EGFR-independent mechanisms, with a major emphasis on chromatin remodeler (SWI/SNF)-related resistance and other therapeutic escape routes. The significance is that mapping these mechanisms can guide development of combination or next-line strategies to overcome osimertinib resistance and improve long-term outcomes.

Guo J, Wen Q, Fan S · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

Dihydroartemisinin inhibits mutant KRAS to potentiate regorafenib plus anti-PD-1 in KRAS-mutant colorectal cancer liver metastases.

This preclinical study tested whether dihydroartemisinin (DHA) can overcome resistance to regorafenib plus anti–PD-1 therapy in KRAS-mutant colorectal cancer liver metastases (CRCLM). It found that KRAS mutation is associated with resistance and that DHA selectively downregulates the KRASG12D mutant without affecting wild-type KRAS, thereby potentiating regorafenib plus anti–PD-1 in the KRAS-mutant setting. These results suggest a targeted combination strategy that exploits KRASG12D vulnerability to improve immunotherapy–TKI efficacy in CRCLM.

Huang N, Wang L, Deng H et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Role of methionine metabolism in cancer: recent advances in molecular mechanisms and therapeutic implications.

This review summarized recent advances in methionine metabolism in cancer, focusing on how methionine uptake/transport and downstream pathways support growth and epigenetic regulation via S-adenosylmethionine. It highlights that many cancers exhibit methionine dependence and that therapeutic targeting of this metabolic vulnerability is promising but limited by tumor heterogeneity and adaptive resistance. Scientifically, it frames methionine-pathway dependencies as actionable stratification biomarkers and therapeutic opportunities across cancer types.

Yang PW, Xu XY, Jiao JY et al. · Experimental hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

MLKL confers ferroptosis resistance in colorectal cancer cells via impaired ESCRT-III-mediated membrane repair.

In colorectal cancer cells, the authors investigated how MLKL (mixed lineage kinase domain-like protein) affects ferroptosis sensitivity and identified the mechanism involving ESCRT-III-mediated membrane repair. They found that MLKL promotes ferroptosis resistance by impairing ESCRT-III-dependent membrane repair processes, thereby altering cellular susceptibility to ferroptotic stress. This mechanistic link positions MLKL and ESCRT-III-mediated repair as potential targets to modulate ferroptosis-based cancer therapies.

Sonkaew S, Duangthim N, Butkinaree C et al. · Biology direct · (2026) · View on PubMed ↗ · Free PDF ↗

Therapeutic activation of PPARα contributes to NOTCH1 inhibition in T-cell acute lymphoblastic leukemia.

The study tested whether therapeutic activation of PPARα with chiglitazar inhibits NOTCH1 signaling in T-cell acute lymphoblastic leukemia (T-ALL) using Jurkat and Molt4 cell lines, mechanistic assays (luciferase reporter, DNA affinity precipitation, co-immunoprecipitation, and ChIP), and mouse xenograft models (CDX and PDX). Chiglitazar treatment reduced T-ALL viability/proliferation and suppressed NOTCH1 pathway activity, with PPARα activation mechanistically contributing to NOTCH1 inhibition. These findings support PPARα as a druggable upstream regulator of NOTCH1 in T-ALL and provide a rationale for PPARα-targeted therapeutic strategies.

Li W, Zhou H, Qin D et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

PD-L1 and PD-L2 regulate in cell-autonomous and N-glycosylation-dependent manners the pro-tumorigenic characteristics and functions of human cancer-associated fibroblasts.

This mechanistic study investigated how PD-L1 and PD-L2 regulate pro-tumorigenic characteristics and functions of human cancer-associated fibroblasts (CAFs) in a cell-autonomous manner and how N-glycosylation controls these effects. Using CAFs derived from breast and lung cancer patients, the study found that PD-L1/PD-L2 signaling and their N-glycosylation-dependent regulation modulate CAF pro-tumorigenic functions and cytokine/immune-interaction phenotypes. The significance is that it links immune checkpoint biology to CAF behavior via glycosylation control, offering potential targets to disrupt tumor-supportive stromal programs.

Abu Raiya A, Meshel T, Kamer I et al. · Molecular medicine (Cambridge, Mass.) · (2026) · View on PubMed ↗ · Free PDF ↗

Foxs1-mediated transformation of CD34+ fibroblast to myCAFs promotes tumor growth.

This study used inducible genetic lineage tracing, single-cell RNA sequencing, and spatial transcriptomics to define the developmental origin and transformation of CD34+ fibroblast progenitors into myCAFs in melanoma and gastric cancer. The key finding was that Cd34+Pi16+ fibroblast progenitors differentiate along a trajectory toward Acta2+ CAFs driven by upregulation of the transcription factor Foxs1, and that this Foxs1-mediated transformation promotes tumor growth. Scientifically and therapeutically, it identifies Foxs1-dependent myCAF generation as a potential target to limit CAF-driven tumor progression.

Yang J, Chen T, Zhang R et al. · EMBO molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

PARG inhibition reduces ssDNA levels and limits RPA loading upon replication fork collapse.

This cellular mechanistic study examined how inhibiting PARG (poly(ADP-ribose) glycohydrolase) affects replication stress responses, focusing on ssDNA accumulation and RPA loading after replication fork collapse. The key finding was that sustained PARylation from PARG inhibition reduces phosphorylated and chromatin-bound RPA most strongly under fork-stalling conditions progressing to fork collapse, requiring PARP1 activity and being modulated by intact ATR–CHK1 checkpoint signaling. This is significant because it clarifies how PARG inhibition reshapes replication fork DNA processing, informing the rationale for PARG-targeted anticancer strategies and combination approaches with checkpoint inhibitors.

Mihuț A, Ghosh D, Kószó A et al. · EMBO reports · (2026) · View on PubMed ↗ · Free PDF ↗

Nanomedicine & Drug Delivery (including EVs/exosomes/nanocarriers)

Systematic evaluation of BBB-penetrant AAV capsids in marmosets identifies VCAP-102 as a highly efficient brain-transducing capsid.

This study systematically evaluated BBB-penetrant AAV capsids in adult marmosets after systemic administration, cross-comparing 11 engineered AAV variants (mostly AAV9-derived) against native AAV9. It identified VCAP-102 as a highly efficient brain-transducing capsid, with whole-brain reporter expression quantified using standardized imaging. The work provides a practical capsid choice for CNS gene delivery and accelerates selection of AAV vectors for translational neurotherapeutic development.

Matsuzaki Y, Konno A, Sakamoto K et al. · Molecular therapy. Advances · (2026) · View on PubMed ↗ · Free PDF ↗

Hypoxia-preconditioned dental pulp stem cells alleviate acetaminophen-induced liver failure via promoting MYC-HIF1A/HIF-1α-BNIP3-mediated mitophagy.

The study investigated whether hypoxia-preconditioned dental pulp stem cells (Hyp-DPSCs) protect against acetaminophen-induced acute liver failure in a therapeutic model. Hyp-DPSCs were reported to alleviate liver injury by promoting MYC–HIF1A/HIF-1α–BNIP3-mediated mitophagy, linking hypoxic conditioning to a specific mitophagy pathway. This mechanistic evidence strengthens the rationale for hypoxia-primed stem cell therapies to treat drug-induced liver injury via targeted mitochondrial quality control.

Li J, Yang Q, Pang P et al. · Autophagy · (2026) · View on PubMed ↗

Hierarchical Flower-Like UiO-66@TiO2 Heterostructure for On-Plate Exosome Enrichment and In Situ Metabolic Fingerprinting Toward Prostate Cancer Diagnosis.

This work developed a hierarchical flower-like UiO-66@TiO2 heterostructure for on-plate exosome enrichment combined with in situ laser desorption/ionization mass spectrometry (LDI-MS) to diagnose prostate cancer. The platform used a ~2 µm high-surface-area architecture for exosome capture and a Type II heterojunction to enhance photothermal conversion, charge transfer, and molecular desorption during LDI-MS. Scientifically and clinically, it provides a liquid-biopsy workflow that couples efficient exosome isolation with metabolic fingerprinting for improved prostate cancer detection.

Jiang X, Zhou Z, Chen L et al. · Small (Weinheim an der Bergstrasse, Germany) · (2026) · View on PubMed ↗

Single-cell transcriptomics-guided dynamic hydrogel delivery of artemisia argyi-derived EVs relieves ER stress and promotes diabetic wound regeneration.

The study used integrated single-cell transcriptomics and multi-omics analyses to characterize immune mechanisms in diabetic wounds and then tested an injectable dynamic hydrogel delivering Artemisia argyi-derived extracellular vesicles (GPOK-2@EVs). It found that endoplasmic reticulum stress (ERS)-related signaling was enriched in pro-inflammatory macrophages in diabetic wounds and that GPOK-2@EVs relieved ER stress and promoted diabetic wound regeneration. This suggests a macrophage-ERS immunomodulation strategy using EV-loaded hydrogels as a potential therapeutic approach for chronic diabetic wound healing.

Miao D, Suo X, Geng X et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Adipocyte-Derived Exosomal Circ_0000002 Affects the Myoblast Growth and Muscle Regeneration.

This study examined whether adipocyte-derived exosomes regulate skeletal muscle development in sheep primary myoblasts (Ovis aries). Co-culture with mature adipocyte exosomes (30–150 nm) increased myoblast proliferation markers (CDK4, PCNA, Cyclin D1) while suppressing differentiation markers (MYOG, MYOD, MYHC). These findings support adipose–muscle exosomal signaling as a potential mechanism to enhance myoblast growth and muscle regeneration in a large-animal model.

Liang L, Zhang W, Yu S et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Butyrylated PGAM5-Triggered and GSH-Responsive Cysteine Polymer Nanoparticles for CBL0137 Delivery to Enhance Necroptosis in Prostate Cancer.

This study developed butyrylated PGAM5-triggered, GSH-responsive cysteine polymer nanoparticles (Cys8E) to deliver the antitumor agent CBL0137 for enhanced necroptosis in prostate cancer models. The Cys8E@CBL nanoparticles exploited high glutathione (GSH) levels to achieve targeted intracellular delivery and improved tumor-killing efficacy, consistent with a necroptosis-enhancing mechanism. The approach suggests a metabolism-responsive nanocarrier strategy to potentiate CBL0137 activity in glutathione-high prostate cancer.

Luo T, Wang L, Cheng B et al. · Advanced healthcare materials · (2026) · View on PubMed ↗

PBAE nanoparticle-mediated delivery of ASCL1 and NGN2 genes for astroglia-to-neuron reprogramming to remodel glial scar for spinal cord injury repair.

This study tested PBAE nanoparticle-mediated delivery of the neuronal reprogramming genes ASCL1 and NGN2 to astroglia for spinal cord injury repair, aiming to remodel glial scar. The approach addresses limitations of viral gene delivery and transplantation by using non-viral gene delivery to drive astroglia-to-neuron reprogramming and reduce persistent glial scar formation. If effective, this gene-delivery strategy could provide a safer, scalable route to promote neuronal replacement after spinal cord injury.

Guo J, Li L, Liu Z et al. · Stem cell research & therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Identification and enrichment of human retinal organoid-derived red/green cone-competent precursors with enhanced axon dynamics.

The study identified and enriched early human retinal organoid-derived red/green (L/M) cone-competent precursor populations with enhanced axon dynamics for potential foveal cone replacement therapy. The authors reported that early L/M cone precursors from developing retinal organoids retain cell-autonomous axonogenesis capacity and can be enriched for superior axon behavior compared with less developmentally competent sources. This is clinically important because it improves the donor-cell quality for integrating transplanted cone precursors into host retina and restoring light-responsive function.

Susaimanickam PJ, Capowski E, Xiong MN et al. · Stem cell research & therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic Disease, Insulin Resistance & Obesity (Mechanisms/Models)

Cardiac myocyte contractility, calcium dynamics, and morphology in Zucker diabetic fatty female and male rats - lacking data in this model of obesity and diabetes: A review.

This Endocrine Regulations review summarizes preclinical evidence on cardiac myocyte contractility, calcium dynamics, and cardiac morphology in Zucker diabetic fatty (ZDF) rats, emphasizing that sex-specific data are limited in this obesity/diabetes model. It frames diabetic cardiomyopathy as a major contributor to diabetes-related mortality and discusses how myocardial structural and functional changes and calcium handling abnormalities may differ by sex. The scientific significance is that it identifies gaps in sex-inclusive mechanistic studies in ZDF rats, guiding more rigorous experimental designs for diabetic cardiomyopathy research.

Zahradnikova A, Ijaz H, Cagalinec M · Endocrine regulations · (2026) · View on PubMed ↗ · Free PDF ↗

The case for primary prevention of obesity in the era of GLP-1 therapies.

This position paper argued for primary prevention of obesity in Europe despite the availability of GLP-1-based pharmacotherapies. It finds that while GLP-1 receptor agonists can produce substantial weight loss and metabolic benefits for individuals, medication access does not remove the need to address obesogenic environments and population-level drivers. The significance is policy and public-health oriented: it supports prioritizing prevention strategies even as effective obesity treatments become more widely available.

Holm S, Tena-Sempere M, Koutsouris D et al. · The Lancet regional health. Europe · (2026) · View on PubMed ↗ · Free PDF ↗

Sub1 contributes to heart failure with preserved ejection fraction driven by aging in mice.

This mouse study examined the role of the transcriptional regulator Sub1 in heart failure with preserved ejection fraction (HFpEF) driven by aging. It found that Sub1 is upregulated in aged hearts and HFpEF models, and that cardiac Sub1 overexpression worsens diastolic dysfunction and accelerates cardiac aging, while Sub1 knockdown delays aging and alleviates HFpEF features even when initiated in aged mice. Mechanistically, Sub1 interacts with TAF9b and AROS to stabilize p53, positioning the Sub1–TAF9b/AROS–p53 axis as a potential therapeutic target for age-associated HFpEF.

Zhao D, Lin L, Zhou Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Liquiritigenin ameliorates adipocyte insulin resistance by inhibiting pro-inflammatory polarization of macrophages via regulation of the mtROS/OXPHOS axis.

Using an HFD-induced obese mouse model plus multi-omics analyses and an in vitro macrophage–adipocyte co-culture system, the study tested liquiritigenin (LQ), a licorice-derived flavonoid, for effects on adipocyte insulin resistance. LQ improved glucose tolerance and insulin sensitivity and ameliorated lipid metabolism by inhibiting pro-inflammatory macrophage polarization through regulation of the mtROS/OXPHOS axis. These mechanistic data support LQ as a candidate metabolic anti-inflammatory compound targeting macrophage mitochondrial ROS/oxidative phosphorylation signaling to treat obesity-related insulin resistance.

Lv C, Tan J, Ouyang H et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Brown Adipose Tissue Secreted Nrg4 Prevents Bone Loss by Orchestrates Bone Resorption and Angiogenesis.

This study used mouse models including brown adipose tissue (BAT) removal, Nrg4 knockout (Nrg4-/-), and BAT transplantation to determine how BAT-secreted Neuregulin 4 (Nrg4) affects bone mass. It found that Nrg4 prevents bone loss by coordinating osteoclastogenesis with angiogenesis–osteogenesis coupling, and it used in vitro assays to test Nrg4 effects on osteoclast formation and vascular–bone interactions. The results identify BAT-derived Nrg4 as a potential therapeutic target for preventing bone loss by orchestrating the resorption–formation and vascular processes that maintain skeletal homeostasis.

Xu X, Zhou J, Tang M et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Diabetes & Cardiovascular Risk Prediction/Prognosis (Cohorts/Markers)

Harnessing Large-Scale Multi-Omics Data for Risk Prediction and Deep Phenotyping of Valvular Heart Diseases in the General Population.

Using UK Biobank data from the general population, this study developed and validated multi-omics risk prediction models for valvular heart disease (VHD) and subtypes (aortic stenosis, aortic regurgitation, mitral regurgitation) with Cox proportional hazards and machine learning methods (XGBoost, LightGBM). Clinical-factor-only Cox models performed best (C-index ~0.75–0.81) and adding proteomic data improved performance (all C-index >0.81), whereas genomic data did not add benefit beyond clinical factors. The scientific significance is that it identifies proteomics as a more informative layer than genomics for deep phenotyping and risk stratification of VHD in community-dwelling individuals.

Jiang Z, Liu Y, Song M et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Impaired fasting glucose is comparable to diabetes mellitus in predicting mortality and cardiovascular events in patients undergoing peritoneal dialysis: the role of β-cell function and insulin resistance.

This prospective cohort study evaluated whether impaired fasting glucose (IFG) predicts mortality and cardiovascular events similarly to diabetes mellitus (DM) in patients undergoing peritoneal dialysis (PD), and assessed roles of β-cell function and insulin resistance. Among 216 PD patients in Taiwan stratified into normal fasting glucose, IFG, and DM groups, β-cell function was measured by HOMA-β and insulin resistance by HOMA-IR. The key implication is that IFG may carry risk comparable to DM in PD, suggesting that β-cell dysfunction and insulin resistance could be important targets for risk stratification and intervention.

Tang CC, Tsai JP, Chen YH et al. · Renal failure · (2026) · View on PubMed ↗ · Free PDF ↗

Joint longitudinal trajectories of the triglyceride-glucose index combined with BMI and waist-to-height ratio and incident cardiovascular disease: a prospective cohort study from the English longitudinal study of ageing.

In a prospective English Longitudinal Study of Ageing cohort of 1808 CVD-free adults aged ≥50 years, researchers modeled joint longitudinal trajectories of the triglyceride-glucose (TyG) index combined with BMI and waist-to-height ratio (WHtR) to predict incident cardiovascular disease. The study identified trajectory groups capturing concurrent changes in metabolic and anthropometric measures and evaluated their associations with future CVD risk. This provides a more dynamic risk stratification framework than single baseline TyG/obesity measures for middle-aged and older adults.

Liu Z, Li Q, Wang B et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Biomarkers for Diabetic Peripheral Artery Disease: An Integrated Review and Clinical Perspective.

This integrated review synthesized PubMed evidence (through December 2025) on biomarkers for diabetic peripheral artery disease (DPA D) in the context of type 2 diabetes mellitus. Across 55 included original studies, it reported dysregulated inflammatory markers (e.g., IL-6, ICAM-1), endothelial/oxidative stress mediators (e.g., TET3, PRDX family), and coagulation markers (e.g., von Willebrand factor, fibrinogen) that correlate with disease severity in comorbid populations. The review highlights a multi-pathway biomarker panel approach for earlier detection and improved risk stratification in DPA D.

Fang L, Ning Q, Wu Y et al. · Diabetes/metabolism research and reviews · (2026) · View on PubMed ↗

Association between HbA1c and red cell distribution width-standard deviation in newly diagnosed, treatment-naïve type 2 diabetes mellitus: a retrospective cross-sectional study.

This retrospective cross-sectional study of 202 newly diagnosed, treatment-naïve adults with type 2 diabetes mellitus (T2DM) examined the association between HbA1c and red cell distribution width-standard deviation (RDW-SD) after adjusting for hematologic, nutritional, renal, and metabolic factors. The key finding was that higher glycemic burden (HbA1c) was associated with RDW-SD, supporting RDW-SD as a potential inflammation/oxidative-stress–linked marker in early untreated T2DM. Scientifically, this links glycemic status to erythrocyte heterogeneity at diagnosis and may help refine risk stratification beyond glucose alone.

Lule KO, Beyaz A, Yildiz H · BMC endocrine disorders · (2026) · View on PubMed ↗ · Free PDF ↗

This multi-center cohort study evaluated whether triglyceride–glucose (TyG)-related indices, the atherogenic index of plasma (AIP), and the cardiometabolic index (CMI) predict adverse cardiovascular events in people with metabolic dysfunction-associated steatotic liver disease (MASLD) versus those classified as non-alcoholic fatty liver disease (NAFLD). The study found that insulin-resistance-related indices (including TyG-related measures, AIP, and CMI) were associated with adverse cardiovascular outcomes and that their predictive performance was compared across the NAFLD-to-MASLD diagnostic transition. These findings support using practical insulin-resistance surrogate markers for cardiovascular risk stratification in MASLD/NAFLD populations, while clarifying how risk prediction may change under updated liver-disease definitions.

Huang Y, Xu Y, Zhang C et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Cardiovascular Disease Prevention & Real-world Comparative Effectiveness

Real-world comparative outcomes of darolutamide- versus abiraterone-based triplet therapy for metastatic hormone-sensitive prostate cancer: a retrospective cohort study.

This retrospective cohort study compared real-world outcomes of darolutamide-based versus abiraterone-based triplet therapy (each combined with ADT and docetaxel) in metastatic hormone-sensitive prostate cancer (mHSPC) using a multinational electronic health record network. It aimed to estimate comparative effectiveness between the two ARPIs in routine practice where head-to-head randomized data are limited. The results are intended to inform treatment selection and expectations for outcomes when choosing darolutamide versus abiraterone in mHSPC.

Chen IA, Chang RI, Yu CC et al. · Therapeutic advances in urology · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative 24-month cardiovascular outcomes and biomarker trajectories with semaglutide, empagliflozin, and sitagliptin in people with obesity and type 2 diabetes: a multicenter real-world study.

This multicenter retrospective real-world study used TriNetX to compare 24-month cardiovascular outcomes and longitudinal biomarker trajectories among adults with obesity and type 2 diabetes treated with semaglutide versus empagliflozin versus sitagliptin. The key finding is that the paper provides comparative evidence over 24 months for both clinical outcomes and biomarker changes across these three active comparators after propensity score matching. Scientifically, it helps determine which incretin-based (semaglutide) or SGLT2-based (empagliflozin) strategies may offer superior cardiovascular risk modification relative to DPP-4 inhibition (sitagliptin) in routine care populations.

Chen JC, Liu KW, Huang YN et al. · Therapeutic advances in endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

The ABCs of cardiovascular disease prevention: communicating what we know in 2026.

This State-of-the-Art review evaluated how to communicate and implement cardiovascular disease (CVD) prevention knowledge in 2026 using the “ABCs of CVD Prevention” framework. It finds that despite advances, control of major risk factors (notably blood pressure and diabetes) has stagnated, and it emphasizes updating and disseminating guideline-based actions to improve uptake. The significance is that a structured communication framework may help translate evidence into population-level prevention strategies amid obesity and aging trends.

Goren LR, Peng AW, Razavi AC et al. · American journal of preventive cardiology · (2026) · View on PubMed ↗ · Free PDF ↗

Synergistic SGLT2 and GLP-1R targeting alleviates systemic inflammation-induced and M1 monocyte-driven endothelial dysfunction in coronary artery disease.

The study tested whether synergistic targeting with an SGLT2 inhibitor and a GLP-1 receptor agonist suppresses systemic inflammation–induced and M1 monocyte-driven endothelial dysfunction in coronary artery disease (CAD). Using analyses of plasma and circulating monocytes across healthy individuals and CAD-related patient groups (with additional cohorts described in the truncated methods), the authors found that combined SGLT2i/GLP-1Ra treatment alleviated monocyte activation and reduced endothelial dysfunction driven by inflammatory mediators and monocytes. This is significant because it identifies a cellular mechanism—monocyte/M1-driven endothelial injury—as a potential basis for the cardiovascular benefits of combined SGLT2 and GLP-1RA therapy.

Mroueh A, Fakih W, Kerth S et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Aging, Biological Age & Longevity Biomarkers/Models

From organ age gaps to precision geromedicine: multi-omic and imaging frameworks for heterogeneous biological aging.

This Review synthesizes evidence on biological aging models built from multi-omic assays (e.g., plasma proteomics, metabolomics, DNA methylation), imaging, and digital/clinical biomarkers, and proposes the ORGAN-AGE interpretive framework for heterogeneous organ-level aging. It finds that many organ- and system-level “biological age” signals are interpreted more strongly than the underlying evidence supports, and clarifies what these signals can versus cannot establish. The work is significant for precision geromedicine because it provides a structured way to judge validity and limitations of multi-modal aging biomarkers across organs and resilience states.

Li QM, Ge XX, Wen TJ et al. · Ageing research reviews · (2026) · View on PubMed ↗

A lipid-sensitive food choice behavior influences aging outcomes from a longevity-promoting diet.

The study examined how lipid-sensitive food choice behavior in the nematode Caenorhabditis elegans affects outcomes from a longevity-promoting Methylobacterium diet. Genetic and sensory analyses identified the AWB/AWC sensory neurons and the odr-1 guanylate cyclase as mediators of aversion, and metabolic profiling linked the avoidance to enriched saturated fats in the Methylobacterium diet. These findings suggest that diet-derived lipid cues can reprogram neuro-sensory feeding decisions and thereby modulate aging trajectories, informing how nutritional composition may influence longevity interventions.

Stuhr NL, Ramos CM, Turner CD et al. · The FEBS journal · (2026) · View on PubMed ↗

This review summarized evidence on how metabolic kinases regulate inter-organelle communication during cellular aging and age-related diseases. It focuses on signaling roles of AMPK, pyruvate dehydrogenase kinases (PDKs), mTOR, AKT, and PERK in coordinating contact and communication among mitochondria, ER, lysosomes, peroxisomes, and the Golgi. The scientific significance is that it frames kinase-driven metabolic control as a unifying mechanism for organelle crosstalk changes that contribute to aging phenotypes and disease progression.

Chowdhury MR, Jeon JH, Chanda D · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Protein lactylation in health and diseases: molecular mechanisms, biological significance, and clinical implications.

This review article examined protein lysine lactylation (Kla), a metabolism–epigenetics post-translational modification, focusing on the enzymatic “writers” (lactyltransferases), “readers,” “erasers” (delactylases), and lactyl-CoA synthases that regulate L-lactylation. It concludes that Kla expands proteome functional diversity beyond histones to non-histone proteins involved in signaling, enzymes, and substrates, with broad implications for health and disease. Clinically, it frames Kla as a potential biomarker and therapeutic target by linking lactate metabolism to gene regulation and disease-relevant pathways.

Yang Y, He Y, Zhang Z et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Multinational cohort study of health perception mismatch trajectories and risks of cognitive decline, depression, and mortality.

This multinational longitudinal cohort study analyzed health perception mismatch trajectories in older adults across CHARLS (China), ELSA (England), and HRS (United States) to assess risks of cognitive decline, depression, and mortality. Distinct mismatch trajectory groups were identified and were associated with subsequent depression, cognitive impairment, and mortality outcomes. The findings support using longitudinal “self-rated health vs functional status” mismatch patterns as prognostic markers for mental health, cognitive decline, and survival in aging populations.

Hu X, Wu Z, Zhang X et al. · BMC public health · (2026) · View on PubMed ↗ · Free PDF ↗

A Melatonin-Catechol Hybrid Molecule Prolongs Lifespan via Regulating ROS and Reprogramming Mitochondrial Metabolism.

This work evaluated the melatonin–catechol hybrid compound MC1 for effects on ROS handling, mitochondrial metabolism, and senescence in oxidative-stress and DNA-damage contexts. MC1 reduced cell senescence and reprogrammed mitochondrial energy metabolism by inhibiting the tricarboxylic acid cycle and glycolysis while promoting fatty acid oxidation, alongside selective regulation of ROS generation. The results suggest MC1 as a candidate longevity/anti-aging therapeutic that targets mitochondrial dynamics and redox balance.

Qian C, Zhang Y, Dang X et al. · Journal of medicinal chemistry · (2026) · View on PubMed ↗

Neurodegeneration & Neuroinflammation (Mechanisms/Targets)

Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1-ALS Autopsy Tissue Donors.

This cross-sectional autopsy case series studied intrathecally administered tofersen distribution in central nervous system tissues from 8 deceased SOD1-ALS autopsy tissue donors. It provides first human estimates of tofersen tissue distribution and corresponding SOD1 reduction in somatic motor system tissues. The scientific and clinical significance is that it links a disease-modifying antisense oligonucleotide therapy (tofersen) to human pharmacodynamic effects in relevant motor pathways.

Guise AJ, Sellon MT, Roemer SF et al. · JAMA neurology · (2026) · View on PubMed ↗

Gene Correction Enhances Dopaminergic Cell Therapy in a Nonhuman Primate Model of Parkinson’s Disease.

The study examined whether CRISPR/Cas9 and prime editing correction of compound LRRK2 mutations (R50H and M2397T) in human iPSC-derived dopaminergic progenitors improves cell therapy in MPTP-lesioned cynomolgus monkeys. Gene-corrected grafts survived for 18 months and expressed dopaminergic markers (TH, GIRK2) with improved maturation compared with uncorrected mutant cells. These findings support LRRK2 gene correction as a potentially safer and more effective strategy for long-term dopaminergic cell replacement in Parkinson’s disease.

Yan Q, Xu C, Gao J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Cholinergic regulation of neuroinflammation: linking microglia, immunometabolism, and neuromodulation.

This review article synthesized evidence on how cholinergic signaling regulates neuroinflammation by linking microglial immune activity with immunometabolism and neuromodulation. It emphasizes the central cholinergic anti-inflammatory pathway as more than the peripheral vagus nerve reflex, highlighting direct CNS interactions between cholinergic neurons and resident microglia. The conceptual framework supports targeting neuromodulatory/cholinergic circuits to modulate microglial inflammatory tone and improve outcomes across neuroinflammatory diseases.

Guo H, Yang Z, Cheng L · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanisms and impact of long COVID: pathophysiology, neuropsychiatric effects and vaccination.

This review examined the pathophysiology and neuropsychiatric effects of long COVID (post-acute sequelae of COVID-19) in COVID-19 survivors, and discussed how vaccination may influence these processes. It reports that long COVID affects an estimated ~1 in 5 COVID-19 survivors and summarizes proposed mechanisms (including immune, autonomic, and neuroinflammatory pathways) alongside common symptoms such as brain fog, dysautonomia, anxiety, depression, and PTSD. The clinical significance is that clarifying mechanisms and the potential role of vaccination could improve risk stratification and targeted management of neuropsychiatric and systemic long COVID sequelae.

Ponnachan P, Dhawlarker A, Yasmin H et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Region-specific features of early glial activation and Aquaporin-4 dysregulation in conditional mouse models of TDP-43 proteinopathies.

This study investigated region-specific early glial activation and aquaporin-4 (AQP4) dysregulation in conditional mouse models expressing human TDP-43 variants (hTDP-43-WT and hTDP-43-ΔNLS) after 1 month of transgene expression. Using immunofluorescence-based analyses, it found that glial activation and AQP4 alterations show region-dependent patterns that differ between nuclear wild-type and cytoplasm-mislocalized TDP-43 expression. The significance is that it links TDP-43 proteinopathy genotype (WT vs ΔNLS) to early neuroinflammatory and water-channel dysregulation, informing mechanistic targets for ALS/FTD-related pathology.

Nieva G, Vassallu F, Depino A et al. · Discovery immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Beyond motor neurons: peripheral TDP-43 pathology in skeletal muscle and intramuscular nerves in amyotrophic lateral sclerosis.

This review summarized evidence that TDP-43 pathology in amyotrophic lateral sclerosis extends beyond motor neurons to peripheral tissues, specifically skeletal muscle and intramuscular nerves. It highlights that phosphorylated TDP-43 deposits have been reported in peripheral compartments in addition to the CNS, supporting a broader view of ALS as a systemic TDP-43 proteinopathy. The significance is that recognizing peripheral involvement may open new avenues for biomarkers and therapeutic targeting outside the central nervous system.

Corti S, Alberti C, Ottoboni L et al. · Brain communications · (2026) · View on PubMed ↗ · Free PDF ↗

Fus-depleted oligodendrocytes reduce neuronal damage and Alzheimer’s disease progression in the AppNL-G-F mouse.

This study tested whether fus-depleted oligodendrocytes can reduce neuronal damage and slow Alzheimer’s disease progression in the AppNL-G-F mouse model. The abstract indicates that oligodendrocyte/myelin dysfunction contributes to AD pathology and that strengthening oligodendrocyte function may preserve neuronal structure and health. If confirmed, the work supports oligodendrocyte-targeted interventions as a mechanistic route to mitigate neurodegeneration and cognitive decline in AD.

Tung TH, Babu S, Tang X et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

This study investigated whether Zika virus (ZIKV) infection induces persistent Alzheimer’s disease-like tau pathology in adult immunocompetent mice across three Collaborative Cross strains. It found that ZIKV drives long-term accumulation of phosphorylated Tau (pTau) associated with impairments in memory and social behavior. These results support a causal viral-to-neurodegeneration mechanism and suggest that ZIKV-triggered tau phosphorylation could model pathways relevant to Alzheimer’s disease.

Calcagno G, Mansuroglu Z, Segrt H et al. · Acta neuropathologica communications · (2026) · View on PubMed ↗ · Free PDF ↗

α-Synuclein triggers intercellular nanotubes formation to prevent apoptosis in astroglia by promoting stemness.

This mechanistic cell biology study examined how α-synuclein (α-SYN) protofibrils affect astroglia survival by inducing tunneling nanotubes (TNTs). It found that α-SYN protofibrils promote TNT formation by inducing aberrant mitochondria with decreased membrane potential and by triggering dynamic actin remodeling through nuclear translocation of phosphorylated focal adhesion kinase (pFAK), which then promotes apoptosis resistance via stemness-associated programs (details truncated). These findings connect α-SYN-driven TNT signaling to astroglial apoptosis resistance, offering potential targets to modulate neuroprotective but disease-relevant astrocyte phenotypes in synucleinopathies.

Kashyap R, Anirudh Sreenivas BK, Varshith MR et al. · Cell & bioscience · (2026) · View on PubMed ↗ · Free PDF ↗

This study investigated whether wasteosome (corpora amylacea) accumulation and regional distribution across neurodegenerative diseases reflect a shared mechanism related to chronic glymphatic insufficiency. It evaluated the compatibility of wasteosome patterns with the proposed role of wasteosomes as markers of impaired glymphatic clearance. The work supports glymphatic dysfunction as a potential unifying upstream driver of wasteosome accumulation in neurodegeneration.

Alsina R, Riba M, Sartorio M et al. · Acta neuropathologica communications · (2026) · View on PubMed ↗ · Free PDF ↗

TDP-43 dysfunction facilitates the pathological conversion of tau.

This study examined whether TDP-43 loss-of-function in forebrain neurons promotes tau pathology by using Tau4R; CaMKII-CreER; Tardbpf/f mice to model TDP-43 dysfunction and tauopathy. TDP-43 LOF exacerbated tauopathy-dependent brain atrophy and increased vulnerability of specific neurons, supporting a role for TDP-43 dysfunction in accelerating pathological tau conversion. The findings are significant because they connect TDP-43 splicing repression failure to worsening tau neurodegeneration, suggesting potential intervention points for co-pathology in neurodegenerative disease.

Baghel MS, Burns GD, Tsapatsis M et al. · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting the cGAS-STING pathway alleviates neuroinflammation and cognitive impairment induced by chronic infection of Toxoplasma gondii.

In a mouse model of chronic Toxoplasma gondii infection, this study assessed activation of the cGAS-STING pathway in the cerebral cortex and tested whether pharmacological inhibition could reverse neuroinflammation and cognitive impairment. The key finding was that chronic infection increased cGAS and STING protein levels and enhanced TBK1/IRF3 phosphorylation, and that inhibiting cGAS-STING alleviated neuroinflammation and improved cognitive outcomes. This supports the cGAS-STING pathway as a therapeutic target for infection-associated neurocognitive disorders driven by sustained neuroinflammation.

Xing Y, Lv H, He P et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Single nuclear RNA sequencing shows altered microglial and astrocytic functions in post-mortem Parkinson’s disease tissue.

This study used single-nuclear RNA sequencing on post-mortem Parkinson’s disease brain tissue to define altered microglial and astrocytic functional programs compared with controls. The key finding was that microglia and astrocytes show disease-associated transcriptional changes consistent with disrupted immune/inflammatory balance in PD. These results are significant because they pinpoint glial molecular pathways that may contribute to neurodegeneration and provide targets for future mechanistic and therapeutic work.

Roy I, Fiorini M, Thomas RA et al. · BMC genomic data · (2026) · View on PubMed ↗ · Free PDF ↗

Neurodevelopmental Disorders & Genetics (ASD/Autism; rare variants)

Diet, gut microbiota, and the gut-brain axis: mechanistic interactions and therapeutic implications in neuropsychiatric disorders.

This mechanistic review synthesized evidence on how diet shapes the gut microbiota and the microbiota–gut–brain axis (MGBA) and how these interactions contribute to neuropsychiatric disorders. It highlights that diet-driven dysbiosis can alter neuroactive metabolite production and intestinal barrier integrity, thereby influencing neuroendocrine and immune signaling linked to conditions such as depression, autism spectrum disorder, Alzheimer’s disease, Parkinson’s disease, and ADHD. The clinical significance is that MGBA components (diet, microbial metabolites, and barrier function) represent potential therapeutic levers for neuropsychiatric disease modification.

Wang X, Piao Y, Xia B et al. · Frontiers in cellular and infection microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Microbiota-gut-brain axis in autism spectrum disorder: integrating brain structure, function, and transcriptomics.

This narrative review synthesized clinical and translational evidence on the microbiota-gut-brain (MGB) axis in autism spectrum disorder (ASD), integrating human cohort/case-control studies, animal models, multi-omics, immune profiling, and multimodal brain assessments (structural/functional MRI and transcriptomics). It reports converging findings that MGB-axis disruption is linked to ASD-relevant neurodevelopmental and neural circuit dysfunction and evaluates microbiota-targeted therapeutic strategies. These integrated mechanistic insights support microbiome-based interventions as potential adjuncts for ASD and highlight transcriptomics and multimodal imaging as key tools for identifying actionable pathways.

Wang G, Liu W, Chen Y et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

RankVar: machine learning-based variant ranking and reinterpretation for rare genetic diseases.

RankVar, a machine learning variant-ranking algorithm, was developed and evaluated using whole-genome/exome sequencing data and clinical notes from rare-disease cohorts (including 260 subjects from the Children’s Hospital of Philadelphia) and training data comprising ~1 million variants from the 1000 Genomes Project with spiked-in pathogenic variants. RankVar used a random forest classifier to prioritize likely causative variants by integrating phenotype information and external biological knowledge with variant features, improving reinterpretation of rare-disease variants across independent datasets. This provides a scalable, knowledge-augmented computational approach to accelerate gene/variant discovery in rare genetic diseases where phenotype-driven variant prioritization is challenging.

Zhang Y, Ahsan MU, Wang P et al. · Genome medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Genetic architecture of patients with autism spectrum disorder - data analysis based on the literature review.

Using a literature review of studies published from 2020 onward, this article analyzed the genetic architecture of autism spectrum disorder (ASD) by compiling reported genetic abnormalities across the ASD population. The key finding was a synthesis of recurring genetic contributors and patterns of genetic variation implicated in ASD, reflecting the heterogeneous genetic basis reported in recent studies. Scientifically, it consolidates current evidence to guide interpretation of ASD genetic findings and highlights the need for continued refinement of genotype–phenotype understanding.

Ręka G, Wojciechowska K, Lejman M · BMC medical genomics · (2026) · View on PubMed ↗ · Free PDF ↗

Neuromuscular & Muscle Regeneration (including exercise/rehab)

Aerobic Exercise and Subthreshold Depressive Symptoms in Adolescents: Secondary Analysis of a Randomized Clinical Trial.

This prespecified secondary analysis of a 12-month, multicenter cluster randomized clinical trial in Chinese adolescents aged 12–17 years evaluated whether aerobic exercise reduces subthreshold depressive symptoms and explored potential neural mechanisms. The key finding (as framed by the study objective) is the association between aerobic exercise and improved subthreshold depressive symptom outcomes, alongside candidate neural mechanisms underlying symptom change. The clinical significance is that it tests an intervention strategy during a developmental window when early treatment could prevent progression to major depression.

Yan X, Shao R, Jin J et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Skeletal muscle biomass as an underappreciated fate of glucose.

This article reviewed evidence that glucose contributes not only to ATP and glycogen in skeletal muscle but also to biomass synthesis in proliferating muscle satellite (stem) cells and during hypertrophy. It highlights mechanisms analogous to anabolic metabolic reprogramming in cancer, including increased glucose uptake, aerobic glycolysis, and TCA-cycle–derived substrates for macromolecule production. The synthesis reframes glucose as a growth substrate in muscle regeneration and hypertrophy, informing future metabolic interventions to enhance muscle growth or repair.

Wackerhage H, Eggelbusch M, Hulmi JJ et al. · American journal of physiology. Cell physiology · (2026) · View on PubMed ↗ · Free PDF ↗

Semaglutide and Musculoskeletal Health: A Mendelian Randomization Study Based on GLP-1 Receptor Expression.

This Mendelian randomization study evaluated whether GLP1R expression (using GLP1R eQTL as instruments) causally affects skeletal and muscle traits relevant to musculoskeletal health, leveraging GWAS summary data. The analysis tested the causal impact of GLP1R modulation on bone and muscle outcomes to infer potential effects of semaglutide, a GLP-1 receptor agonist. If consistent with the MR direction, the findings would clarify whether semaglutide is likely to benefit or harm musculoskeletal health via GLP1R-mediated pathways.

Li D, Liang X, Li Z et al. · Endocrine, metabolic & immune disorders drug targets · (2026) · View on PubMed ↗

Systemic regeneration medicines for muscular dystrophy: progress and challenges in pro-regenerative drug development.

This review examined progress and challenges in developing pro-regenerative drugs for muscular dystrophy, focusing on strategies to enhance intrinsic skeletal muscle regeneration rather than relying solely on cell transplantation. It highlights histone deacetylase (HDAC) inhibitors as a compelling example of pharmacologic approaches aimed at improving regenerative capacity. The review underscores key translational hurdles and opportunities for drug-based regenerative therapies in muscular dystrophy.

Fukada SI, Kubo A, Kanagawa M et al. · Cell regeneration (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

The effect of eccentric phase tempo on acute neuromechanical responses and short-term post-exercise recovery in healthy trained and recreationally active adults: a systematic review.

This systematic review synthesized evidence from eccentric-only and eccentric-phase-tempo–manipulated resistance exercise protocols in healthy adults (including competitive athletes, resistance-trained individuals, and recreationally active participants) to determine how eccentric phase duration affects acute neuromuscular fatigue, exercise-induced muscle damage markers, and recovery up to 7 days. Across included studies, the review evaluated whether controlled eccentric-phase tempo produces distinct acute neuromechanical responses and short-term post-exercise recovery patterns. The work is significant for optimizing resistance-training prescription by linking eccentric tempo parameters to fatigue/damage and recovery outcomes.

Matuszczyk F, Wilk M, Fostiak K et al. · BMC sports science, medicine & rehabilitation · (2026) · View on PubMed ↗ · Free PDF ↗

Infectious Disease Epidemiology, Vaccines & Antimicrobials

Acute Pancreatitis Induced by Rhinovirus Infection.

This report described acute pancreatitis occurring in the context of rhinovirus infection. The abstract provides no experimental or mechanistic details beyond the clinical association. Scientifically, it highlights a potential viral trigger for pancreatitis that warrants further investigation into causality and underlying pathways.

Sajjad MM, Abujazar MYO, Al-Mutairi GT · Journal of the College of Physicians and Surgeons—Pakistan : JCPSP · (2026) · View on PubMed ↗ · Free PDF ↗

Association between probiotic, prebiotic, and yogurt consumption and colorectal cancer: real-world evidence from the US NHANES.

This NHANES-based real-world study analyzed adults aged 50+ (2001–2020) to test associations between probiotic, prebiotic, and yogurt consumption and colorectal cancer (CRC) prevalence. It reports an epidemiologic link between intake of these microbiota-modulating foods and CRC prevalence (details truncated in the abstract). If confirmed, these findings would support dietary microbiome modulation as a potentially actionable, population-level factor in CRC risk reduction.

Tu CW, Wang HL · Nutrition & diabetes · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of higher-dose versus lower-dose corticosteroids in community-acquired pneumonia: a systematic review and network meta-analysis.

This systematic review and frequentist network meta-analysis compared higher-dose versus lower-dose adjunctive corticosteroids in hospitalized patients with community-acquired pneumonia (CAP), using dexamethasone-equivalent thresholds (high ≥7.5 mg/day vs low <7.5 mg/day). It synthesized randomized controlled trials up to January 25, 2026, with short-term all-cause mortality as the primary outcome. The clinical significance is that it aims to clarify whether dose escalation of corticosteroids provides additional mortality benefit, informing dosing decisions in CAP care.

Ouyang Y, Lai J, Wang P et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Influenza Vaccine Effectiveness Against Pediatric Death in the United States: 2016-2025.

Using a case-cohort design, this study estimated influenza vaccine effectiveness (VE) against influenza-associated pediatric death in the United States from 2016–2017 through 2024–2025 among children <18 years. It compared vaccination status among reported pediatric deaths with survey-based estimates of seasonal influenza vaccination coverage. The results quantify how well seasonal influenza vaccination prevents the most severe outcome—death—in pediatric populations across multiple seasons.

Leonard JS, Reinhart K, Lu PJ et al. · Pediatrics · (2026) · View on PubMed ↗

Characteristics of Streptococcus pneumoniae colonising Cypriot children during a period of high PCV10 and PCV13 vaccine coverage: serotypes and antimicrobial resistance.

This cross-sectional study characterized nasopharyngeal carriage of Streptococcus pneumoniae in Cypriot children aged 6 months to 6 years during a period of high PCV10 and PCV13 vaccine coverage, assessing serotypes and antimicrobial resistance. Using cultured isolates confirmed by PCR and multiplex PCR/latex agglutination serotyping, the study identified the circulating pneumococcal serotypes and their resistance profiles in the vaccinated pediatric population. The findings are significant for understanding vaccine-driven shifts in pneumococcal epidemiology and for informing local antimicrobial resistance surveillance and vaccine policy.

Ioannou Vassiliadou G, Ladas P, Mendris M et al. · BMC infectious diseases · (2026) · View on PubMed ↗ · Free PDF ↗

Synergistic anti-Helicobacter pylori efficacy of a molecularly identified Limosilactobacillus fermentum isolate in combination with multiple antibiotics.

This experimental study screened 40 lactic acid bacteria (LAB) isolates for anti–Helicobacter pylori activity against 20 clinical H. pylori isolates and then tested synergistic efficacy of a molecularly identified Limosilactobacillus fermentum isolate combined with multiple antibiotics. The key finding was that the identified L. fermentum strain enhanced anti–H. pylori effects when used in combination with antibiotics, supporting a synergistic approach against resistant gastric infection. Clinically, this suggests a potential adjunct strategy to improve eradication outcomes in the setting of rising H. pylori antibiotic resistance.

Ali MMMM, Shady HMA, M SM et al. · BMC microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Host-Pathogen Immunity & Antiviral Mechanisms

CAMKV is an ISG and facilitates the degradation of rabies virus phosphoprotein via SQSTM1-mediated selective autophagy.

This study identified CAMKV as an interferon-stimulated gene (ISG) that suppresses rabies virus replication by promoting degradation of the rabies virus phosphoprotein (P). CAMKV was shown to interact with rabies P and the autophagy receptor SQSTM1, driving SQSTM1-mediated selective autophagic clearance of P in vitro, and CAMKV overexpression delayed disease progression in mice challenged with a street rabies strain. The findings position CAMKV–SQSTM1 selective autophagy as a host antiviral mechanism and a potential target for therapeutic strategies against rabies.

Wang J, Huo H, Tao Y et al. · Autophagy · (2026) · View on PubMed ↗

Pre-treatment Gut Microbiome Diversity and Function Linked to Cytotoxic and Natural Killer Cell Immune Responses after N-803 Treatment in People with HIV.

This exploratory longitudinal metagenomic study profiled fecal microbiomes from 10 ART-suppressed people with HIV at multiple timepoints before, during, and after treatment with N-803, an IL-15 superagonist. Although overall taxonomic and functional diversity did not significantly change, beneficial microbial taxa and pathways were nominally enriched after N-803, including a nominal increase in Faecalibacterium prausnitzii. The work links N-803 immunotherapy to gut microbiome shifts that may help explain or enhance cytotoxic and natural killer (NK) immune responses in HIV.

Chakrawarti A, Cromarty RT, Basting CM et al. · Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · (2026) · View on PubMed ↗ · Free PDF ↗

A receptor-Fc based SFV replicon Trim-Away platform for targeted viral protein degradation.

This study developed a receptor-Fc based SFV replicon Trim-Away platform that uses TRIM21-mediated ubiquitination to target viral proteins for degradation. By fusing engineered receptor-Fc proteins to the E3 ligase TRIM21, the system enabled highly specific intracellular recognition and degradation of targeted viral proteins. This provides a programmable antiviral strategy that may reduce resistance compared with conventional inhibitors by eliminating viral proteins rather than blocking their activity.

Han Y, Dong Q, Tian Z et al. · Virology journal · (2026) · View on PubMed ↗ · Free PDF ↗

GSK’872 mitigates ischemia-reperfusion injury in rat lung transplants by regulating PANoptosis and inflammation in cell type specific manner.

The study tested whether the RIPK3 inhibitor GSK’872 mitigates ischemia-reperfusion injury (IRI) in a rat lung transplant model, using human lung transplant IRI single-cell RNA-seq data to define cell-type-specific death and inflammation pathways. GSK’872 reduced IRI-related injury and modulated PANoptosis and inflammatory responses in a cell type–specific manner, consistent with targeting RIPK3-dependent necroptosis-linked pathways. This provides preclinical evidence that RIPK3 inhibition via GSK’872 could be a therapeutic strategy to improve lung transplant outcomes by limiting combined cell death and inflammation.

Li J, Ma X, Huang J et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

Overcoming the bottleneck in Treponema pallidum quantification: a novel flow cytometric assay for rapid, precise, and cost-effective detection.

This methodological study developed a novel flow cytometric assay to overcome the bottleneck in quantifying Treponema pallidum for rapid, precise, and cost-effective detection. The key advance was integrating direct detection speed with flow-cytometry throughput and precision, addressing limitations of dark-field microscopy (low sensitivity/reproducibility) and quantitative PCR (time-consuming and reagent-dependent). Scientifically, the assay can accelerate studies of syphilis pathogenesis, treatment response monitoring, and vaccine development by enabling more scalable T. pallidum quantification.

Zeng YL, Xu WL, Xiao Y et al. · BMC microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Autoimmunity, Inflammation & Immune Profiling (non-cancer)

This JAMA Review summarizes epidemiology, risk thresholds, clinical spectrum, and management considerations for alcohol-related liver disease (ALD) in humans. It emphasizes that ALD can range from reversible steatosis to steatohepatitis and more severe liver injury, with commonly cited daily ethanol thresholds (e.g., >20 g/day for women and >30 g/day for men) associated with risk. The clinical significance is that it consolidates evidence to support prevention, diagnosis, and treatment decisions for a leading cause of liver morbidity and mortality and a major indication for liver transplantation.

Krag A, Åberg F, Mellinger J et al. · JAMA · (2026) · View on PubMed ↗

Deep Immunophenotyping Reveals Distinct Immune Signatures in Axial Spondyloarthritis and Psoriatic Arthritis.

This study compared immune cell subsets, activation/differentiation markers, and cytokine profiles between patients with axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA) using spectral flow cytometry of PBMCs from 179 patients and 49 healthy donors. It identified distinct disease-specific immune signatures across the two conditions, indicating immunophenotypic divergence within the spondyloarthritis spectrum. The results suggest that immune profiling could help stratify patients and potentially guide differential therapeutic response in axSpA versus PsA.

Frede N, Craig-Müller N, Kohrt S et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗ · Free PDF ↗

Early response toward clinical remission with dupilumab in severe asthma: Real-world cohort.

This multicenter prospective real-world cohort study evaluated early response toward clinical remission at 24 weeks after starting dupilumab in adults with severe asthma across 13 Japanese institutions. It assessed whether dupilumab leads to an early remission trajectory and identified baseline factors associated with achieving this outcome. The findings help define early predictors of remission with dupilumab, supporting more timely treatment evaluation in severe asthma.

Mizumura K, Gon Y, Tanaka A et al. · The journal of allergy and clinical immunology. Global · (2026) · View on PubMed ↗ · Free PDF ↗

FcRn antagonist and C5 complement inhibitor as early rescue strategies in severe Myasthenia Gravis: a two-case report.

This two-case report described early rescue strategies in severe generalized AChR-antibody–positive myasthenia gravis (MG) using an FcRn antagonist and a C5 complement inhibitor. In both cases, early initiation of these advanced therapies was associated with rapid clinical stabilization in patients refractory to standard immunosuppression. The report provides preliminary clinical support for prompt use of FcRn and complement blockade in complex severe MG scenarios, warranting further systematic study.

Parisi M, Molitierno N, Alberti C et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

This pharmacovigilance study assessed real-world drug-related bone metabolism disorders by integrating FDA FAERS (2004–2024) and VigiAccess data with a Bradford Hill-based causal plausibility framework. Using four disproportionality algorithms—ROR, PRR, BCPNN, and MGPS—it screened for and evaluated signals suggesting causal plausibility for adverse bone remodeling outcomes linked to drugs. The scientific significance is that it provides a scalable method to identify and prioritize potential drug safety risks for osteoporosis/osteomalacia/rickets using large-scale post-marketing surveillance data.

Liu P, Zhao K, Zhang H et al. · Frontiers in pharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Stapokibart provides significant improvements in signs and symptoms of atopic dermatitis irrespective of prior systemic treatment: a post-hoc analysis of a phase 3 trial.

This post-hoc analysis evaluated stapokibart (CM310AD005) in adults with moderate-to-severe atopic dermatitis, comparing efficacy and safety in systemic treatment–naïve versus previously treated patients. At week 16, stapokibart 600 mg loading followed by 300 mg every 2 weeks produced significantly higher EASI-75 and EASI-90 response rates than placebo in systemic treatment–naïve patients, with benefits reported irrespective of prior systemic treatment history. Clinically, the results support stapokibart as an effective option for atopic dermatitis across treatment backgrounds, potentially simplifying therapeutic positioning in real-world care.

Zhao Y, Zhang L, Wu L et al. · The Journal of dermatological treatment · (2026) · View on PubMed ↗ · Free PDF ↗

This phase 2b, double-blind, randomized, placebo-controlled single-center trial (MADAI) tested propionic acid (PA) as an add-on therapy in 101 adults with clinically stable multiple sclerosis. The trial evaluated PA’s efficacy and safety over the study period in a randomized comparison versus placebo. If effective, PA supplementation could represent a microbiome-derived metabolite strategy to modulate immune and neuronal pathways in multiple sclerosis.

Moser T, Hitzl W, Lerda-Casaccia T et al. · Brain : a journal of neurology · (2026) · 1 citations · View on PubMed ↗

Testicular malakoplakia in a middle-aged Han Chinese male: a case report and review of the literature.

This case report described testicular malakoplakia in a 41-year-old middle-aged Han Chinese male and reviewed the literature, focusing on diagnostic imaging features. The patient presented with right scrotal swelling and systemic urinary/inflammatory symptoms, and the report aimed to clarify contrast-enhanced ultrasound (CEUS) manifestations to avoid misdiagnosis as testicular tumor. Clinically, it emphasizes that rare granulomatous lesions like malakoplakia can mimic malignancy and that CEUS may help improve diagnostic accuracy.

Ruan Z, Ma X, Chen Y et al. · Journal of medical case reports · (2026) · View on PubMed ↗ · Free PDF ↗

Parabens exposure in systemic lupus erythematosus: insights from network toxicology and molecular docking.

This study investigated whether parabens exposure is linked to systemic lupus erythematosus (SLE) by mapping paraben-associated target genes to SLE-related genes using network toxicology and functional enrichment. Shared paraben–SLE genes were analyzed with GO and KEGG to identify candidate pathways and molecular mechanisms potentially connecting parabens to immune dysregulation in SLE. The work supports a hypothesis-generating framework for environmental contribution to autoimmunity and highlights molecular targets for future experimental validation.

Li H, Guo Q, Zhang T et al. · BMC pharmacology & toxicology · (2026) · View on PubMed ↗ · Free PDF ↗

Longitudinal immune-inflammatory profiles and mortality in older adults with sepsis: a multicentre prospective cohort study.

In a multicentre prospective cohort, immune-inflammatory profiles were characterized across the older adult infection spectrum (healthy controls, nonsevere infection, and sepsis) in 1,851 participants aged ≥60 years, with longitudinal assessment of in-hospital mortality. The study found immune-cell subset, cytokine, complement, and routine laboratory patterns that distinguished sepsis from nonsevere infection and that longitudinal immune-inflammatory trajectories were associated with mortality risk. These findings suggest that dynamic immune-inflammatory profiling could improve prognostic stratification in older adults with sepsis.

Wang X, Fu M, Li C et al. · Journal of intensive care · (2026) · View on PubMed ↗ · Free PDF ↗

Nutritional status in pediatric celiac disease: evaluation at diagnosis and during follow-up.

This pediatric celiac disease study measured anthropometric parameters and micronutrient levels at diagnosis and again at 6 and 12 months after starting a gluten-free diet (GFD), and assessed associations with tissue transglutaminase IgA (tTG-IgA). The key finding was the pattern of nutritional recovery (or persistent deficiencies) over the first year on GFD and how these changes related to serologic activity reflected by tTG-IgA. Clinically, it supports monitoring growth and micronutrients during follow-up to identify children who may need targeted nutritional or adherence interventions.

Yılmaz S, Çam Sİ · BMC nutrition · (2026) · View on PubMed ↗ · Free PDF ↗

Sex differences in non-reproductive cancers: mechanistic roles of sex-hormone signaling.

This review examined mechanistic roles of sex-hormone signaling in sex differences observed across non-reproductive cancers, focusing on tumor-intrinsic and tumor microenvironment pathways. It highlights that ER, AR, and PR drive classical nuclear transcriptional programs, while membrane/cytoplasmic receptor pools and GPER enable rapid non-genomic signaling through PI3K/AKT and MAPK/ERK pathways. The synthesis is significant for understanding why outcomes differ by sex and for informing sex-informed therapeutic strategies targeting hormone signaling.

Xu J, Zhang X, Li Z et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

Dysregulated glia and periglomerular cells in the olfactory bulb and altered lipocalins in the olfactory epithelium underlie olfactory dysfunction in a murine model of eosinophilic chronic rhinosinusitis.

The study investigated how type 2 inflammation in eosinophilic chronic rhinosinusitis (ECRS) alters the olfactory bulb and olfactory epithelium in a murine model, linking dysregulated glia/periglomerular cells to olfactory dysfunction and assessing altered lipocalins in the olfactory epithelium. Using a calcipotriol plus ovalbumin topical sensitization for 14 days followed by intranasal ovalbumin challenge, the authors found histopathological and molecular changes consistent with glial/periglomerular dysregulation and lipocalin alterations associated with impaired olfaction. These results are significant because they provide mechanistic targets in central and peripheral olfactory compartments for ECRS-related smell loss.

Kagoya R, Nishijima H, Horikiri K et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of GLP-1RA on blood eosinophil levels in adults: a real-world study.

In a retrospective single-center real-world study in Shanghai, China, the authors evaluated adults newly prescribed the GLP-1 receptor agonist semaglutide to determine effects on blood eosinophil levels and to identify clinical/metabolic determinants of eosinophil reduction. Semaglutide treatment was associated with changes in eosinophil counts, and the study analyzed baseline characteristics and metabolic factors linked to the magnitude of eosinophil decrease. This is significant because it provides real-world evidence for GLP-1RA effects on eosinophilic inflammation, relevant to asthma and other eosinophil-driven conditions.

Wu Y, Lin Y, Wu J et al. · BMC pulmonary medicine · (2026) · View on PubMed ↗ · Free PDF ↗

An AI-augmented review of childhood atopic dermatitis biomarkers across genetic, immune, microbial, and metabolic domains.

This AI-augmented review synthesized childhood atopic dermatitis biomarker evidence across genetic, immune, microbial, and metabolic domains. The key finding was an integrated, systems-level comparison that distinguishes evidence strength and highlights how biomarker signals differ across molecular layers and study contexts. This is significant for improving how clinicians and researchers prioritize biomarkers for validation and for making the rapidly expanding AD literature more navigable than traditional manual reviews.

Lee JW, Loo EXL, Chong SS et al. · Molecular medicine (Cambridge, Mass.) · (2026) · View on PubMed ↗ · Free PDF ↗

Reproductive/Endocrine & Women’s/Men’s Health Biomarkers

Association Between Serum Follicle-Stimulating Hormone Levels and Risk of Diabetes in Middle-Aged Men: A Long-Term Population-Based Longitudinal Study.

This longitudinal population-based study assessed whether baseline serum follicle-stimulating hormone (FSH) levels predict incident type 2 diabetes (T2DM) in 1097 middle-aged and older men from the Tehran Lipid and Glucose Study. Using multivariable logistic and Cox regression over 3774.78 person-years, it found an association between serum FSH and both prevalent and future T2DM risk. Clinically, FSH could serve as a biomarker for diabetes risk stratification in men, linking reproductive hormone signaling to metabolic disease development.

Mousavi M, Firouzi F, Ramezani Tehrani F et al. · Endocrinology, diabetes & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Nonsteroidal anti-inflammatory drug resistance in dysmenorrhea: a study of prevalence, predictors, and alternative pain management among Nigerian female students.

This cross-sectional study in 271 Nigerian female undergraduate students at Afe Babalola University, Ado-Ekiti (ABUAD) assessed the prevalence of nonsteroidal anti-inflammatory drug (NSAID)–resistant dysmenorrhea, predictors of inadequate NSAID response, and alternative pain management strategies. The key finding was that a substantial subset of participants experienced inadequate pain relief despite NSAID use, and the study identified factors associated with NSAID resistance and patterns of alternative management. Clinically, this supports the need for improved dysmenorrhea screening and tailored pain-management approaches beyond standard NSAID therapy in young women.

Orok E, Aremu B, Iheme C et al. · Reproductive health · (2026) · View on PubMed ↗ · Free PDF ↗

EMBRACE COMPASS: protocol for a multi-country cross-sectional comparative analysis of pregnancy and postnatal care architecture.

This paper presents the protocol for EMBRACE COMPASS, a multi-country cross-sectional comparative analysis designed to map pregnancy and postnatal care architecture for gestational diabetes, hypertensive disorders of pregnancy, perinatal depression, and uncomplicated pregnancy. Using a structured, multi-layered care architecture framework, the study will compare how different health-system designs and implementation features relate to care delivery patterns across countries. The significance lies in enabling systematic, cross-national benchmarking of maternity care systems to support evidence-based improvements in maternal and perinatal outcomes.

Arechvo A, Crisan A, Wang Y et al. · BMC pregnancy and childbirth · (2026) · View on PubMed ↗ · Free PDF ↗

Comparison of genetic profile and kidney outcomes between very early-onset and non-very-early-onset autosomal dominant polycystic kidney disease in children: a systematic review and meta-analysis.

This systematic review and meta-analysis compared genetic profiles and kidney outcomes between very early-onset autosomal dominant polycystic kidney disease (VEO-ADPKD; onset in utero or within 18 months) and non-very-early-onset ADPKD in children under 18 years. The analysis synthesized radiologic and clinical outcome data to determine whether the VEO subgroup shows a distinct genetic pattern and a more severe renal disease course than later-onset pediatric ADPKD. Clinically, the results help refine prognosis and risk counseling for children with early-onset ADPKD and guide expectations for disease progression based on onset timing and genotype.

Kapogiannis C, Dimakopoulos G, Kapogiannis A et al. · BMC nephrology · (2026) · View on PubMed ↗ · Free PDF ↗

Generated automatically on July 07, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.

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PubMed Trending Research Digest — July 07, 2026

PubMed Trending Research Digest — July 07, 2026

Overview

Immunotherapy & Cancer Clinical Trials (Checkpoint/Antibody/ADC/Combination)

Cisplatin-gemcitabine-durvalumab reintroduction in advanced biliary tract cancer: a multinational real-world analysis.

Polatuzumab Vedotin Plus Rituximab, Gemcitabine, and Oxaliplatin in Relapsed or Refractory Diffuse Large B-Cell Lymphoma: Results From the Phase III, Randomized POLARGO Trial.

Next-Generation Checkpoint Combinations: Optimizing PD-(L)1-Based Therapy Across the Advanced, Adjuvant, and Neoadjuvant Settings.

Carfilzomib, lenalidomide, and dexamethasone (KRd) versus bortezomib, lenalidomide, and dexamethasone (VRd) induction prior to autologous haematopoietic stem cell transplant/transplantation in newly diagnosed multiple myeloma.

Orelabrutinib versus chemoimmunotherapy in treatment-naïve chronic lymphocytic leukemia/small lymphocytic lymphoma: a randomized, phase 3 trial.

Durvalumab with gemcitabine-based chemotherapy regimens in advanced biliary tract cancer: primary results from the phase IIIb TOURMALINE study.

Advances in antibody-drug conjugates in cancer: latest updates from the 2026 AACR annual meeting.

Targeted Protein Degradation (PROTACs) & Epigenetic Targets

Discovery of SD-2301 as a Highly Potent and Selective PROTAC STAT3 Degrader Capable of Achieving Complete Tumor Regression with Single Administration.

GID4-Recruiting PROTACs for BRD4 Degradation Overcome Resistance Driven by CRBN and VHL Deficiency.

Cancer Cell Mechanisms & Therapeutic Resistance (Non-clinical)

SEPTIN7 Enhances Tumorgenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling.

Development and Validation of a Pathomics Model for Prognosis Prediction in Neoadjuvant Therapy-Treated Breast Cancer: A Retrospective, Multicenter Study.

Osimertinib Resistance in EGFR-Mutated Non-Small Cell Lung Cancer: Mechanisms and Therapeutic Strategies.

Dihydroartemisinin inhibits mutant KRAS to potentiate regorafenib plus anti-PD-1 in KRAS-mutant colorectal cancer liver metastases.

Role of methionine metabolism in cancer: recent advances in molecular mechanisms and therapeutic implications.

MLKL confers ferroptosis resistance in colorectal cancer cells via impaired ESCRT-III-mediated membrane repair.

Therapeutic activation of PPARα contributes to NOTCH1 inhibition in T-cell acute lymphoblastic leukemia.

PD-L1 and PD-L2 regulate in cell-autonomous and N-glycosylation-dependent manners the pro-tumorigenic characteristics and functions of human cancer-associated fibroblasts.

Foxs1-mediated transformation of CD34+ fibroblast to myCAFs promotes tumor growth.

PARG inhibition reduces ssDNA levels and limits RPA loading upon replication fork collapse.

Nanomedicine & Drug Delivery (including EVs/exosomes/nanocarriers)

Systematic evaluation of BBB-penetrant AAV capsids in marmosets identifies VCAP-102 as a highly efficient brain-transducing capsid.

Hypoxia-preconditioned dental pulp stem cells alleviate acetaminophen-induced liver failure via promoting MYC-HIF1A/HIF-1α-BNIP3-mediated mitophagy.

Hierarchical Flower-Like UiO-66@TiO2 Heterostructure for On-Plate Exosome Enrichment and In Situ Metabolic Fingerprinting Toward Prostate Cancer Diagnosis.

Single-cell transcriptomics-guided dynamic hydrogel delivery of artemisia argyi-derived EVs relieves ER stress and promotes diabetic wound regeneration.

Adipocyte-Derived Exosomal Circ_0000002 Affects the Myoblast Growth and Muscle Regeneration.

Butyrylated PGAM5-Triggered and GSH-Responsive Cysteine Polymer Nanoparticles for CBL0137 Delivery to Enhance Necroptosis in Prostate Cancer.

PBAE nanoparticle-mediated delivery of ASCL1 and NGN2 genes for astroglia-to-neuron reprogramming to remodel glial scar for spinal cord injury repair.

Identification and enrichment of human retinal organoid-derived red/green cone-competent precursors with enhanced axon dynamics.

Metabolic Disease, Insulin Resistance & Obesity (Mechanisms/Models)

Cardiac myocyte contractility, calcium dynamics, and morphology in Zucker diabetic fatty female and male rats - lacking data in this model of obesity and diabetes: A review.

The case for primary prevention of obesity in the era of GLP-1 therapies.

Sub1 contributes to heart failure with preserved ejection fraction driven by aging in mice.

Liquiritigenin ameliorates adipocyte insulin resistance by inhibiting pro-inflammatory polarization of macrophages via regulation of the mtROS/OXPHOS axis.

Brown Adipose Tissue Secreted Nrg4 Prevents Bone Loss by Orchestrates Bone Resorption and Angiogenesis.

Diabetes & Cardiovascular Risk Prediction/Prognosis (Cohorts/Markers)

Harnessing Large-Scale Multi-Omics Data for Risk Prediction and Deep Phenotyping of Valvular Heart Diseases in the General Population.

Impaired fasting glucose is comparable to diabetes mellitus in predicting mortality and cardiovascular events in patients undergoing peritoneal dialysis: the role of β-cell function and insulin resistance.

Joint longitudinal trajectories of the triglyceride-glucose index combined with BMI and waist-to-height ratio and incident cardiovascular disease: a prospective cohort study from the English longitudinal study of ageing.

Biomarkers for Diabetic Peripheral Artery Disease: An Integrated Review and Clinical Perspective.

Association between HbA1c and red cell distribution width-standard deviation in newly diagnosed, treatment-naïve type 2 diabetes mellitus: a retrospective cross-sectional study.

Comparative performance of insulin resistance-related indices in predicting adverse cardiovascular events among individuals with NAFLD and MASLD: a multi-center cohort study.

Cardiovascular Disease Prevention & Real-world Comparative Effectiveness

Real-world comparative outcomes of darolutamide- versus abiraterone-based triplet therapy for metastatic hormone-sensitive prostate cancer: a retrospective cohort study.

Comparative 24-month cardiovascular outcomes and biomarker trajectories with semaglutide, empagliflozin, and sitagliptin in people with obesity and type 2 diabetes: a multicenter real-world study.

The ABCs of cardiovascular disease prevention: communicating what we know in 2026.

Synergistic SGLT2 and GLP-1R targeting alleviates systemic inflammation-induced and M1 monocyte-driven endothelial dysfunction in coronary artery disease.

Aging, Biological Age & Longevity Biomarkers/Models

From organ age gaps to precision geromedicine: multi-omic and imaging frameworks for heterogeneous biological aging.

A lipid-sensitive food choice behavior influences aging outcomes from a longevity-promoting diet.

Metabolic Kinases as Regulators of Inter-Organelle Communication in Aging and Age-Related Diseases.

Protein lactylation in health and diseases: molecular mechanisms, biological significance, and clinical implications.

Multinational cohort study of health perception mismatch trajectories and risks of cognitive decline, depression, and mortality.

A Melatonin-Catechol Hybrid Molecule Prolongs Lifespan via Regulating ROS and Reprogramming Mitochondrial Metabolism.

Neurodegeneration & Neuroinflammation (Mechanisms/Targets)

Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1-ALS Autopsy Tissue Donors.

Gene Correction Enhances Dopaminergic Cell Therapy in a Nonhuman Primate Model of Parkinson’s Disease.

Cholinergic regulation of neuroinflammation: linking microglia, immunometabolism, and neuromodulation.

Mechanisms and impact of long COVID: pathophysiology, neuropsychiatric effects and vaccination.

Region-specific features of early glial activation and Aquaporin-4 dysregulation in conditional mouse models of TDP-43 proteinopathies.

Beyond motor neurons: peripheral TDP-43 pathology in skeletal muscle and intramuscular nerves in amyotrophic lateral sclerosis.

Fus-depleted oligodendrocytes reduce neuronal damage and Alzheimer’s disease progression in the AppNL-G-F mouse.

Zika virus infection induces a persistent accumulation of Alzheimer’s disease-like Tau phosphorylation in adult immunocompetent mice in association with memory and social behavior impairments.

α-Synuclein triggers intercellular nanotubes formation to prevent apoptosis in astroglia by promoting stemness.

Regional wasteosome accumulation across neurodegenerative diseases points to a shared underlying mechanism potentially related to glymphatic insufficiency.

TDP-43 dysfunction facilitates the pathological conversion of tau.

Targeting the cGAS-STING pathway alleviates neuroinflammation and cognitive impairment induced by chronic infection of Toxoplasma gondii.

Single nuclear RNA sequencing shows altered microglial and astrocytic functions in post-mortem Parkinson’s disease tissue.

Neurodevelopmental Disorders & Genetics (ASD/Autism; rare variants)

Diet, gut microbiota, and the gut-brain axis: mechanistic interactions and therapeutic implications in neuropsychiatric disorders.

Microbiota-gut-brain axis in autism spectrum disorder: integrating brain structure, function, and transcriptomics.

RankVar: machine learning-based variant ranking and reinterpretation for rare genetic diseases.

Genetic architecture of patients with autism spectrum disorder - data analysis based on the literature review.

Neuromuscular & Muscle Regeneration (including exercise/rehab)

Aerobic Exercise and Subthreshold Depressive Symptoms in Adolescents: Secondary Analysis of a Randomized Clinical Trial.