PubMed Trending Research Digest — September 28, 2026

Automated digest · 97 articles · 15 research areas · September 28, 2026

Overview

This week’s digest is dominated by mechanistic biology that links cellular stress pathways to disease outcomes—especially via mitochondria, immune signaling, and microenvironmental cues. Multiple studies emphasize how mitochondrial control systems and redox/metabolic states act as “decision points” for survival versus regulated cell death (e.g., metabolite–mitochondrial quality control coupling; mitochondrial Ca2+ homeostasis; and mitochondrial protease/FAO–ferroptosis axes). In parallel, neuroimmune and inflammatory circuits recur across contexts: microglial TREM2/cGAS–STING signaling, mast cell regulation by epidermal immune axes, and obesity- and smoking-associated inflammatory triggers that converge on inflammasomes, pyroptosis, and immune dysfunction.

On the translational side, several papers focus on precision stratification and therapy selection using modern data modalities. Proteomics/phosphoproteomics reveal molecular endotypes in advanced heart failure; spatial proteomics is paired with explainable graph neural networks to extract prognostic tissue patterns; and imaging- or biomarker-driven tools are proposed to guide immunotherapy decisions (including AI models for hepatocellular carcinoma and multimodal frameworks for cancer immunotherapy response). In parallel, clinical implementation studies (e.g., lecanemab in routine care; neuromodulation rankings in Alzheimer’s; and real-world treatment comparisons in cardiac amyloidosis) highlight the growing emphasis on feasibility, safety monitoring, and phenotype-specific evidence.

Finally, infectious and respiratory themes remain prominent, spanning host–pathogen invasion dependencies (Toxoplasma rhoptry discharge; chikungunya replication factors) and viral immune mechanisms (EBV immunopathology and vaccine epitope mapping; influenza NS1–PARP1 condensate control of transcriptional pausing). Public health and stewardship angles also appear through coordinated forecasting of influenza/COVID-19/RSV seasonality and evidence-based causality frameworks for infection-associated inflammatory diseases. Together, the set underscores a broader trend: integrating mechanistic insight with quantitative, phenotype-aware tools to improve prevention, diagnosis, and targeted therapy.

---

Host–Pathogen Interactions & Invasion Mechanisms

Chikungunya virus uses the tetraspanins CD63, CD9, and CD151 to replicate in human synovial fibroblasts.

This study investigated host dependency factors for chikungunya virus (CHIKV) replication in primary human synovial fibroblasts, focusing on the 19 tetraspanins and exosome-associated tetraspanins CD63, CD9, and CD151. Silencing CD63 and CD151 reduced CHIKV subgenomic replicon activity, CD9 localized near replication sites and its silencing reduced intracellular CHIKV genome accumulation, and silencing all three tetraspanins decreased progeny virus production. These results identify CD63/CD9/CD151 as functional host factors for CHIKV replication in joint cells, informing potential therapeutic targets to limit arthritogenic alphavirus infection.

Brown EK, Stegmann C, Biermann H et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Defining the essential genome of diverse phages with phage Tn-seq.

This study developed and applied phage Tn-seq to define the essential genome of diverse bacteriophages, using Tn5 transposon mutagenesis with anti-CRISPR-based selection followed by deep sequencing. It found that phage Tn-seq worked across diverse phages (including a nucleus-forming jumbo phage), enabled gene essentiality assignment consistent with structural proteomics and core gene conservation, and used insertion biases to predict transcriptional features. The scientific significance is that this genome-wide, unbiased approach accelerates phage engineering and supports phage-based antimicrobial development by identifying essential genes and functional genomic regions.

Kyte N, Fuchs M, Smith LM et al. · Nature microbiology · (2026) · View on PubMed ↗

Clustering of host N-glycans by the microneme MIC1/4/6 complex licenses Toxoplasma rhoptry discharge.

This study investigated how host N-glycans and cholesterol biosynthesis regulate rhoptry discharge during Toxoplasma gondii invasion using a host cell–directed genome-wide screen and microneme MIC1/4/6 complex–dependent mechanisms in host cells. The key finding was that clustering of host N-glycans by the Toxoplasma MIC1/4/6 microneme complex is required to license normal rhoptry discharge, with host N-glycosylation and cholesterol biosynthesis pathways emerging as essential. This mechanistic insight identifies host glycosylation and lipid pathways as actionable determinants of parasite invasion and provides targets for interventions against toxoplasmosis.

Valleau D, Goyal M, Roberts JM et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cardiac Proteomics/Phosphoproteomics & Molecular Endotypes

Cardiac proteomic and phosphoproteomic profiling defines clinically relevant molecular subgroups in human heart failure.

This study profiled left ventricular tissue from 149 patients with advanced heart failure across nine clinical etiologies using cardiac proteomics and phosphoproteomics to define molecular subgroups. Despite convergence to a shared end-stage proteomic landscape by etiology, unbiased proteome-based clustering identified two molecular subgroups with distinct remodeling phenotypes, including differences in fibrosis and immune cell infiltration, supported by consistent phosphoproteomic stratification. Clinically, these data suggest that proteome-defined molecular endotypes may better stratify patients than etiology alone and could improve biomarker development and therapy targeting in heart failure.

Hamed O, Reitz CJ, Kuzmanov U et al. · Nature cardiovascular research · (2026) · 1 citations · View on PubMed ↗

---

Circadian Timing & Chronotherapy in Exercise

Exploring the adoption of wearable physical activity monitoring technology amongst older adults in Hong Kong: a grounded theory approach.

This grounded theory qualitative study explored attitudes and experiences of older adults in Hong Kong who used wearable physical activity monitoring technology (WPAMT) for at least 30 days. Most participants reported positive attitudes and willingness to continue, with perceived usefulness, versatility, importance, convenience, and effectiveness driving continued use, while negative attitudes were linked to perceptions that the technology was challenging, unnecessary, and unaffordable. Understanding these determinants can improve design and implementation strategies to increase sustained adoption of WPAMT in older populations.

Man SS, Su P, So BCL et al. · Ergonomics · (2026) · View on PubMed ↗

Beyond jump height: monitoring countermovement jump metrics across the Anterior Cruciate Ligament rehabilitation journey.

This article discussed how to monitor countermovement jump (CMJ) metrics across the anterior cruciate ligament (ACL) rehabilitation journey, addressing challenges in selecting force-platform-derived metrics and interpreting them over time. The key finding was that different CMJ-derived metrics provide different information, so practitioners should choose metrics based on objective markers and the rehabilitation goal rather than relying on jump height alone. Clinically, it supports more consistent, evidence-informed CMJ monitoring to track functional recovery and readiness during ACL rehab.

Bishop C, Maestroni L, Bettariga F et al. · Physiotherapy theory and practice · (2026) · View on PubMed ↗

Effects of Heat-Killed Bifidobacterium breve B-3, a Postbiotic, on Muscle Mass-Related Parameters in Patients with Sarcopenia: A Randomized, Double-Blind, Placebo-Controlled Pilot Trial.

This randomized, double-blind, placebo-controlled pilot trial tested heat-killed Bifidobacterium breve B-3 (B-3HK; 2×10^10 cells/day) in adults aged 50–89 years with AWGS 2019-defined sarcopenia. The study’s key finding (as reported in the abstract) was the evaluation of B-3HK’s effects on muscle mass-related parameters, with the primary endpoint being change in knee extension strength over 24 weeks. Scientifically, it explores whether a postbiotic can serve as an adjunct to improve functional muscle outcomes in established sarcopenia.

Asaoka D, Yoshimoto S, Katsumata N et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of Daily Rhythm-Aligned Training on Skeletal Muscle Adaptation in Older Adults: A Randomized Controlled Trial.

This randomized controlled trial studied whether resistance training aligned to an individual’s daily peak time of day versus trough time improves skeletal muscle adaptation in older adults. The key finding was that rhythm-aligned training produced greater skeletal muscle adaptations than training performed at the trough time (with the trial comparing three arms over the intervention period). Scientifically and clinically, the results support incorporating circadian timing into exercise prescriptions to better counter age-related sarcopenia risk.

Bruggisser F, Ritter S, Roth R et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

---

Immunotherapy for Cancer (Biomarkers, AI, and Decision Support)

A Multi-Targeting Chimeric Antigen Receptor-T Cell Platform to Overcome Antigen Heterogeneity in the Treatment of Non-Small Cell Lung Cancer.

The study developed and tested a multi-targeting “Bicephali” CAR-T platform for non-small cell lung cancer (NSCLC) to overcome antigen heterogeneity and T cell exhaustion. The Bicephali CAR-T uses a dual-transmembrane design with two extracellular antigen-binding domains targeting CD276 and NKG2D ligands (NKG2DLs) while sharing a 4-1BB/CD3ζ intracellular signaling domain, and it showed superior tumor killing versus conventional BB002 CAR-T in vitro and in vivo. This supports multi-antigen CAR design as a strategy to improve efficacy against heterogeneous solid-tumor antigen landscapes.

Wang L, Zhang Y, Peng S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Transformer-Based Multitask Framework Integrating Habitat and Deep Learning for Predicting Early Disease Control and Survival in Immunotherapy-Treated Hepatocellular Carcinoma.

This study developed and validated ECOS-Net, a transformer-based multitask model integrating CT-derived habitat features and 2.5D deep learning features to predict early disease control (DC) and overall survival (OS) in immunotherapy-treated hepatocellular carcinoma (HCC) patients. In 832 ICI-treated patients used for model development (from 1,234 total across eight institutions/databases), ECOS-DC achieved AUCs around 0.82–0.84 across training, internal validation, and external testing, with the model generating early DC probabilities and OS risk scores via multi-head attention. Clinically, this provides an imaging-based decision-support tool for stratifying ICI response and prognosis in heterogeneous HCC populations.

Fu X, Guo Y, Gong B et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

SpaCEy links spatial tissue patterns to clinical outcomes using explainable graph neural networks.

SpaCEy, an explainable graph neural network, was developed to link spatial proteomics tissue patterns to clinical outcomes in datasets with overall survival endpoints. The model represents tissues as spatial graphs from molecular marker expression without predefined cell-type labels or anatomical regions and identifies tissue intercellular/molecular patterns predictive of survival. This provides a clinically interpretable way to extract prognostic spatial biomarkers from spatial omics for patient stratification.

Rifaioglu AS, Ervin EH, Sarigun A et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Overall and Line-Specific Impact of Targeted Therapies in Advanced Biliary Tract Cancer After Chemoimmunotherapy Failure.

This retrospective international study analyzed 1,358 patients with advanced biliary tract cancer treated with first-line cisplatin, gemcitabine, and durvalumab to determine how matched targeted therapy after chemoimmunotherapy failure affects outcomes by treatment line. Using ESCAT tier I actionable alterations, the study compared matched targeted therapy with active non-targeted treatment and reported line-specific impacts on post-progression outcomes (abstract truncated). The results inform which patients and which post-progression lines may benefit most from precision-matched targeted agents after chemoimmunotherapy.

Rimini M, Ikeda M, Abidoye O et al. · Journal of hepatology · (2026) · View on PubMed ↗

Reassessing the Clinical Value of Momelotinib in Myelofibrosis: An ESMO-MCBS:H-Based Appraisal of SIMPLIFY-1 and MOMENTUM.

This appraisal evaluated the clinical value of momelotinib in myelofibrosis by reviewing evidence from the SIMPLIFY-1 and MOMENTUM trials using the ESMO Magnitude of Clinical Benefit Scale for Haematological Malignancies (ESMO-MCBS:H). The key conclusion was a critical reassessment of momelotinib’s magnitude of benefit—particularly relevant because momelotinib (a JAK1/JAK2 and ACVR1 inhibitor) is intended to improve splenomegaly and anemia via hepcidin suppression. The review helps clinicians and payers judge whether momelotinib provides clinically meaningful benefit beyond existing JAK inhibitor options.

Wever SAL, Hoogendoorn M, Klein SK et al. · Critical reviews in oncology/hematology · (2026) · View on PubMed ↗ · Free PDF ↗

Drosophila midgut tumor-induced insulin resistance systemically remodels lymph gland hematopoiesis during cancer cachexia.

This study used a Drosophila larval cancer cachexia model by expressing yki3SA in adult midgut precursors (AMP) to generate a midgut tumor and induce insulin resistance, then examined systemic effects on lymph gland hematopoiesis. Tumor-induced cachexia remodeled hematopoietic niche function and caused aberrant blood cell differentiation in the lymph gland, linking peripheral insulin resistance to immune/hematopoietic dysregulation. These findings clarify how nonautonomous tumor signals reprogram circulating immune cell development during cachexia, offering mechanistic targets for cachexia-associated immune dysfunction.

Chowdhury U, Panzade G, Karnik PN et al. · The FEBS journal · (2026) · View on PubMed ↗

New advances in the treatment of chronic rhinosinusitis with nasal polyps from pathophysiology to biologic targeted therapy.

This narrative review summarized the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP), emphasizing type 2 inflammation pathways (IL-4, IL-13, IL-5, IgE, and TSLP) and the clinical evidence for biologic targeted therapies. The key finding was that biologics directed at these type 2 inflammatory mediators can address underlying immune dysregulation and reduce recurrence risk compared with traditional approaches alone. Clinically, it provides an evidence-based roadmap for precision biologic selection in CRSwNP patients with type 2–driven disease.

Huang B, Xu Y, Tian Y et al. · Frontiers in allergy · (2026) · View on PubMed ↗ · Free PDF ↗

Trial design drives outcomes: harmonising efficacy across BCG-unresponsive bladder carcinoma in situ trials.

This study examined how trial design heterogeneity affects reported efficacy across single-arm registrational trials of BCG-unresponsive carcinoma in situ (CIS) of the bladder by reconstructing survival data from six trials and running simulation analyses. The key finding was that differences in response assessment protocols—such as biopsy timing, complete response (CR) definitions, retreatment policies, and handling of withdrawals—substantially altered efficacy estimates. Scientifically and clinically, it highlights that apparent treatment performance in BCG-U CIS trials may be driven partly by methodology, underscoring the need for harmonized endpoints.

Robesti D, Kamat AM, Ploussard G et al. · BJU international · (2026) · View on PubMed ↗ · Free PDF ↗

Selinexor potentiates NK cell activation against multiple myeloma.

This experimental immunology study tested whether selinexor, a selective inhibitor of nuclear export targeting XPO1, potentiates NK cell activation against multiple myeloma using MM cell lines and primary myeloma cells from patients. The key finding was that selinexor enhanced NK-cell–relevant immune activation in the presence of tumor microenvironment cues (e.g., IFNγ or IL-6), including measurable changes in HLA-E and functional immune readouts. Clinically, it supports selinexor as an immunomodulatory strategy that could improve NK-mediated anti-myeloma activity.

Harding DT, Graham LV, Bartlett LG et al. · Clinical and experimental immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Virotherapy for Spinal and Spinal Cord Tumors: Current Evidence and Future Perspectives.

This review studied oncolytic virotherapy for spinal and spinal cord tumors, summarizing current evidence for tumor-selective oncolytic viruses (including adenovirus, herpes simplex virus, and reovirus) and their ability to induce systemic antitumor immunity. It concludes that while the rationale is strong for sparing surrounding neural tissue, clinical data specifically in spinal/spinal cord indications remain limited. Scientifically, it frames future directions for translating oncolytic virus platforms into more effective local and immune-mediated therapies for otherwise difficult-to-treat spinal tumors.

Uotani K, Fujiwara T, Takatori R et al. · Microorganisms · (2026) · View on PubMed ↗ · Free PDF ↗

Two Decades of NPM1-Mutated Acute Myeloid Leukemia: From Molecular Insights to Clinical Decision-Making.

This narrative review studied NPM1-mutated acute myeloid leukemia (AML) over two decades, focusing on how molecular insights have shifted clinical decision-making. It reports that management has evolved from early immunohistochemical observations of aberrant cytoplasmic NPM1 localization to modern genetics-based stratification and measurable residual disease (MRD)-driven approaches, with prognostic impact shaped by co-occurring genetic alterations. The significance is that updated NPM1-centered molecular and MRD frameworks can improve risk assessment and guide treatment intensity in this distinct AML subtype.

Cimino G, Caridi M, Celenza R et al. · Cancers · (2026) · View on PubMed ↗ · Free PDF ↗

Prognostic Role of Adverse Events in a Worldwide Population of Patients with Biliary Tract Cancer Treated with Chemo-Immunotherapy.

This retrospective international cohort study examined whether immune-mediated adverse events (imAEs) predict outcomes in patients with biliary tract cancer (BTC) treated with first-line cisplatin–gemcitabine plus durvalumab. The key finding is that occurrence of imAEs was analyzed as a treatment-emergent correlate of immune activation with prognostic relevance for overall survival (OS) and progression-free survival (PFS). If validated, imAE occurrence could serve as a practical biomarker to identify BTC patients more likely to benefit from chemo-immunotherapy.

Bartalini L, Rimini M, Ikeda M et al. · Cancers · (2026) · View on PubMed ↗ · Free PDF ↗

The Significance of Somatic Variants Involved in the Development of Pancreatic Cancer in Patients with HBOC-Associated Germline Variants.

This study investigated how combinations of germline hereditary breast and ovarian cancer (HBOC)–associated variants and tumor somatic variants relate to pancreatic cancer development using tumor–normal paired comprehensive genomic profiling (CGP) in patients carrying HBOC germline variants. It found that specific somatic variant patterns, when interpreted alongside the patients’ germline HBOC variants, can help explain heterogeneity in pancreatic cancer development beyond germline status alone. This is clinically significant because it supports more personalized cancer risk assessment and surveillance strategies for HBOC carriers by incorporating tumor somatic context.

Uchiyama K, Nishikubo H, Sano T et al. · Genes · (2026) · View on PubMed ↗ · Free PDF ↗

External validation of the NADIR model for early prostate-specific antigen response prediction in enzalutamide-treated metastatic hormone-sensitive prostate cancer: An analysis of the ARCHES trial.

This analysis externally validated the NADIR (nadir androgen receptor pathway inhibitor) model for predicting early favorable prostate-specific antigen (PSA) response in enzalutamide-treated metastatic hormone-sensitive prostate cancer (mHSPC) using data from the ARCHES trial. In 574 enzalutamide-treated patients (558 with complete predictors), the locked NADIR model’s discrimination, calibration, and prediction accuracy metrics were assessed to determine whether it reliably predicts PSA decline to ≤0.2 ng/mL by 6 months. The clinical significance is that a validated early-response model can support earlier treatment stratification and decision-making in mHSPC receiving enzalutamide.

Roy S, Armstrong AJ, Agarwal N et al. · Cancer · (2026) · View on PubMed ↗

GLP-1 Receptor Agonists in Heart Failure: A Systematic Review and Meta-analysis with Phenotype-Specific Effects and Dual Analytical Frameworks.

This systematic review and meta-analysis studied glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in heart failure (HF), evaluating treatment effects across HF phenotypes using both trial-level and phenotype-based analytical frameworks. It found that GLP-1 RA effects on cardiovascular outcomes vary by HF phenotype and that integrating heterogeneous trial populations improves interpretability of benefits and risks. The significance is that phenotype-specific evidence can guide more precise consideration of GLP-1 RA use in HF populations.

Yuan Y, Chen C, Li X et al. · Drugs · (2026) · View on PubMed ↗

Efficacy and Safety of Risankizumab in Paediatric Patients With Psoriasis in the OptIMMize-1 Phase III Study.

This phase III OptIMMize-1 study evaluated the efficacy and safety of the IL-23 inhibitor risankizumab versus ustekinumab (and subsequent randomized/withdrawal components) in pediatric patients with moderate-to-severe psoriasis over 52 weeks. The key finding was that risankizumab demonstrated clinically meaningful efficacy with an acceptable safety profile through one year in the pediatric population. This supports risankizumab as a potential advanced biologic option for children and adolescents with psoriasis who need more effective systemic therapy.

Magnolo N, Lara WL, Reich A et al. · The British journal of dermatology · (2026) · View on PubMed ↗ · Free PDF ↗

Emerging advances in multimodal AI in cancer immunotherapy: from multi-scale data integration to clinical decision support.

This review assessed emerging multimodal AI approaches for cancer immunotherapy, focusing on methods for multi-scale data integration and clinical decision support to address resistance and relapse after immunotherapy. The key finding was that conventional biomarkers often lack predictive accuracy and transferability, and that multimodal AI can better capture tumor–immune dynamics by integrating diverse data types. The clinical significance is that these AI frameworks may enable more robust, personalized prediction of immunotherapy response and guide treatment selection across cancer types.

Zhang W, Luo Z, Liu K et al. · Science bulletin · (2026) · View on PubMed ↗ · Free PDF ↗

---

Mitochondrial Quality Control, Metabolism & Cell Death

Persistent Zn2+ Influx-Mediated Deacetylation of ANXA2 Regulates the “Zn2+-Autophagic Flux” and Alleviates Intervertebral Disc Degeneration.

The study explored the molecular mechanism by which zinc imbalance and autophagy disruption contribute to intervertebral disc degeneration (IVDD), integrating single-cell RNA-seq, mRNA-seq, and LC-MS to identify key regulators. It identified the zinc transporter ZIP14 (SLC39A14) and showed that persistent Zn2+-influx–mediated deacetylation of annexin A2 (ANXA2) at lysine 302 (K302) regulates the “Zn2+-autophagic flux,” thereby alleviating IVDD. These results connect ZIP14-driven Zn2+ signaling to ANXA2 post-translational control of autophagy, suggesting a zinc–ANXA2 axis as a therapeutic target for IVDD.

Jin Y, Chen Y, Xie Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

SIRT5-Mediated Desuccinylation of ACAA2 Protects Against Calcium Oxalate-Induced Kidney Injury by Regulating Fatty Acid Oxidation to Suppress Mitochondrial Oxidative Injury and Ferroptosis.

This study examined how SIRT5-mediated desuccinylation in renal tubular epithelial cells (RTECs) affects calcium oxalate (CaOx) crystal–induced kidney injury in human samples and mouse models. SIRT5 was reduced in CaOx stones and models, and multi-omics (succinylomics/lipidomics/proteomics) showed that SIRT5 preserves fatty acid oxidation (FAO) by desuccinylating FAO enzymes, with SIRT5 deficiency causing PUFA accumulation, phospholipid remodeling, mitochondrial oxidative injury, and ferroptosis. These findings identify SIRT5 as a mechanistic regulator of FAO–ferroptosis coupling and suggest SIRT5-targeted strategies to prevent nephrolithiasis-associated renal damage.

Jiang Q, Dong C, Liu Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Hyaluronic Acid-PEG-PLGA Nanoparticles Encapsulating Myricetin Attenuate NMDA-Induced Retinal Ganglion Cell Injury Associated with Microglia-Related Neuroinflammatory Responses.

This study investigated whether hyaluronic acid–PEG–PLGA nanoparticles encapsulating myricetin (MY) can protect retinal ganglion cells (RGCs) from NMDA-induced injury by modulating microglia-related neuroinflammation. The authors formulated MY-loaded nanoparticles (MY-NPs) and evaluated their effects on nanoparticle properties and neuroprotective outcomes in an NMDA excitotoxicity model, targeting microglial inflammatory responses that amplify neuronal damage. The significance is a drug-delivery strategy that improves aqueous delivery of myricetin and may reduce excitotoxic, inflammation-driven retinal neurodegeneration.

Yang X, Xu J, Long L et al. · International journal of nanomedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Claudin-5 regulates mitochondrial bioenergetics and protects the heart against myocardial infarction.

The authors investigated whether cardiomyocyte Claudin-5 (Cldn5) regulates mitochondrial bioenergetics and protects against myocardial infarction using human heart tissue localization and HL-1 cardiomyocyte siRNA knockdown. Cldn5 localized to mitochondria, and Cldn5 knockdown reduced mitochondrial number, increased the ADP/ATP ratio, and accelerated mitochondrial reactive oxygen species accumulation. This suggests an intracellular Cldn5–mitochondria axis as a potential target for cardioprotection in myocardial infarction.

Yu X, Chen B, Wang L et al. · Biochimica et biophysica acta. Molecular basis of disease · (2026) · View on PubMed ↗

CLPP loss confers sex-specific protection from renal ischemia reperfusion injury.

This study examined how loss of the mitochondrial matrix protease CLPP affects renal ischemia-reperfusion injury (IRI) in mice, with sex-specific analyses of mitochondrial redox responses and tubular damage. CLPP deficiency reduced succinate-driven mitochondrial H2O2 production and protected kidneys from functional decline, tubular necrosis, mitochondrial ultrastructural injury, and lipid peroxidation after IRI, with the strongest protection observed in females. These findings identify CLPP as a sex-influenced regulator of mitochondrial redox resilience and suggest CLPP-targeted strategies could mitigate IRI-related acute kidney injury.

Isermann L, Rojas-Morales P, Senft K et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗

Nanopore direct RNA sequencing and the epitranscriptome: Advances in mapping native RNA landscapes.

This iMeta review summarized advances in nanopore direct RNA sequencing (DRS) and how it maps native RNA landscapes and the epitranscriptome. The key technical finding is that DRS enables single-molecule, long-read sequencing of native RNA without reverse transcription or amplification, allowing simultaneous detection of multiple RNA modifications, full-length transcript architecture, alternative splicing, and poly(A) tail features. This synthesis highlights how nanopore DRS can accelerate mechanistic studies of RNA regulation and modification in health and disease.

Zhang T, Li J, Tang C et al. · iMeta · (2026) · 3 citations · View on PubMed ↗ · Free PDF ↗

Mitochondrial Ca2+ homeostasis in ovarian function and oocyte competence: from molecular transporters to early embryonic development.

This review article synthesized evidence on how mitochondrial Ca2+ transporters and regulators (including the mitochondrial calcium uniporter complex with MICU1, MICU2, and EMRE, and the Na+/Ca2+ exchanger NCLX) shape ovarian cell signaling, energy metabolism, redox balance, and oocyte competence, with implications for early embryonic development. The key finding was that transient mitochondrial Ca2+ uptake promotes oxidative phosphorylation and survival pathways, whereas sustained Ca2+ accumulation drives ROS generation, mitochondrial permeability transition, and cell death. Scientifically, it clarifies molecular mechanisms linking mitochondrial Ca2+ homeostasis to fertility and provides a framework for targeting transporter/regulator pathways to improve oocyte quality.

Fu X, Huang Q, Wu H et al. · Frontiers in cell and developmental biology · (2026) · View on PubMed ↗ · Free PDF ↗

Spatiotemporal Dynamics of Protein Recruitment During Cell Wound Repair.

This preprint investigated the molecular recruitment dynamics that occur during cell wound repair, focusing on how proteins are spatially and temporally organized as cells reseal ruptured plasma membranes and underlying cortical cytoskeleton. The key finding was that protein recruitment during wound repair follows distinct spatiotemporal patterns rather than a uniform response. Scientifically, it advances mechanistic understanding of cellular repair processes that are relevant to tissue injury, infection, and disease contexts such as cancer.

Nakamura M, Hui J, Verboon JM et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolite Regulation of Mitochondrial Quality Control and Regulated Cell Death.

This review examined how specific metabolites—β-hydroxybutyrate (β-BHB), lactate, succinate, and acetate—regulate mitochondrial quality control and regulated cell death by integrating redox, mitochondrial integrity, organelle turnover, and renewal pathways. The key finding was that mitochondrial quality control acts as a gating layer that translates metabolite-dependent redox and acylation signals into cell-fate decisions between recovery and regulated cell death. The scientific significance is that metabolite–MQC coupling provides a framework for understanding variable stress responses and for designing metabolism-targeted strategies to modulate cell death in disease.

Hu J, Hu C, Chen Y et al. · Antioxidants & redox signaling · (2026) · View on PubMed ↗

---

Publication Bias & Research Translation (Bibliometrics)

10-year analysis of selective dissemination in glaucoma research from major conferences to journals.

This bibliometric analysis studied publication outcomes of glaucoma research by tracking full-text publication rates of abstracts presented at major international conferences (AGS, EGS, ICGS, WGC) from 2010–2020 and relating them to journal impact factors and study characteristics. The key finding was that determinants such as study design and other abstract-level features were associated with the likelihood of full-text publication and that publication venues varied in impact factor. Scientifically, the work highlights publication bias and can inform how conference findings translate into peer-reviewed evidence in glaucoma research.

Ghirardi A, Camisa L, De Cillà S et al. · The British journal of ophthalmology · (2026) · View on PubMed ↗

---

Cancer Therapeutics Targeting Adhesion & Microenvironment

High-Density Type I Collagen Promotes IFN-γ+ CD8+ T Cell Exhaustion via SAT1-ASS1-Mediated Glutamine Accumulation and Ferroptosis in Triple-Negative Breast Cancer.

The study examined how extracellular matrix remodeling—specifically high-density type I collagen—affects immune cell fate in triple-negative breast cancer (TNBC) by combining patient correlation analyses with transcriptomics/metabolomics and in vitro functional experiments. High-density type I collagen promoted IFN-γ+ CD8+ T cell exhaustion through SAT1–ASS1–mediated glutamine accumulation and ferroptosis, linking ECM mechanics to immunosuppressive metabolism and cell death. This provides a mechanistic rationale for targeting the collagen–SAT1/ASS1–ferroptosis axis to improve anti-tumor T cell function in TNBC.

Wang J, Pan S, Bai L et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

PTBP1-Mediated Alternative Splicing of DNAJB6 Promotes Everolimus Resistance in Clear Cell Renal Cell Carcinoma via EIF4B/PKIB/AKT/mTOR Positive Feedback Loop.

The study investigated how PTBP1-driven alternative splicing of DNAJB6 contributes to everolimus (EVE) resistance in clear cell renal cell carcinoma (ccRCC) and how this rewires AKT/mTOR signaling. It showed that PTBP1 promotes EVE resistance via an EIF4B/PKIB/AKT/mTOR positive feedback loop, supported by single-cell transcriptomics linking PTBP1 expression with resistance-associated pathway activity and by patient-derived and in vivo/in vitro validation. These findings identify PTBP1–DNAJB6 splicing and the EIF4B/PKIB/AKT/mTOR loop as actionable targets to overcome everolimus resistance.

Pan XW, Zheng HF, Li MC et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Integrated Multi-Omics Reveals Cellular States and Microenvironmental Remodeling in Coexisting DCIS and IDC.

The study characterized cellular states and microenvironmental remodeling during progression from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) by integrating spatial transcriptomics, single-cell RNA-seq, and single-cell DNA-seq on coexisting DCIS and IDC samples. It identified candidate progression-limiting genes including MGP, PLAT, and SERPINA3 and delineated malignant epithelial meta-programs associated with distinct transcriptional states between DCIS and IDC. This multi-omics framework highlights specific molecular candidates that may constrain or predict the DCIS-to-IDC transition.

Zhang N, Wan T, Zhang S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Dual Compartmentalization of GSTA4 Suppresses Ferroptosis to Drive Antiandrogen Resistance in Prostate Cancer.

The study investigated mechanisms of antiandrogen resistance in castration-resistant prostate cancer (CRPC) by integrating multi-omics analyses of resistant models and patient specimens. It identified glutathione S-transferase alpha 4 (GSTA4) as a key ferroptosis suppressor and showed that its dual compartmentalization enables detoxification of the lipid peroxidation product 4-hydroxynonenal, thereby driving resistance to antiandrogen therapy. These findings suggest that disrupting GSTA4 compartment-specific ferroptosis suppression could restore ferroptosis sensitivity and counter antiandrogen resistance.

Luo Y, Zhuang W, Li Z et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Advances in Drug Delivery Systems for Breast Cancer: From Microenvironment Barriers and Smart Carriers to Clinical Translation Strategies.

This review article surveyed advances in drug delivery systems (DDS) for breast cancer, focusing on how tumor microenvironment barriers and smart carrier designs affect delivery and clinical translation. It synthesized evidence that collagen networks, pH/glutathione (GSH) gradients, and tumor-associated macrophages (TAMs) limit penetration and efficacy, and it outlined formulation/manufacturing considerations needed for translation. Scientifically, it provides a structured roadmap for designing next-generation breast cancer DDS that overcome microenvironment-driven resistance.

Liang G, Zhu C, Sun H et al. · Drug design, development and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

In vivo assessment of broccoli extract based hydrogel in mitigating DMBA induced breast cancer in female mice.

This preclinical study evaluated a broccoli extract-loaded hydrogel as a localized delivery platform to mitigate DMBA-induced breast cancer in female BALB/c mice. The key finding was that hydrogel-based delivery of broccoli extract (rich in sulforaphane) improved outcomes in the DMBA mammary tumor model compared with untreated controls, consistent with antioxidant, anti-inflammatory, pro-apoptotic, and antiproliferative activity. These findings support further development of sulforaphane-containing biomaterial formulations as potentially safer, targeted breast cancer therapeutics.

Parashar K, Khan MA, Verma M et al. · Frontiers in oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Broad targeting of the cell adhesion machinery - cancer cell detachment triggered by the alpha1-oleate complex.

The study investigated intravesical alpha1-oleate treatment in bladder cancer patients and validated its effects in cellular models using assays of cell-adhesion machinery. Alpha1-oleate broadly inhibited multiple adhesion families by targeting claudins and focal-adhesion constituents, disrupting tight junctions, focal adhesions, and adherens junctions while sparing gap junctions and desmosomes in a dose-dependent manner. This suggests alpha1-oleate as a potential non-genetic, adhesion-targeting therapeutic strategy to promote tumor cell detachment and reduce tumor burden in bladder cancer.

Chaudhuri A, Haq F, Ambite I et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗ · Free PDF ↗

---

Clinical Case Reports in Critical Care/Oncology

A case report on the management of sepsis complicated by eroded mixed hemorrhoids following breast cancer chemotherapy.

This case report described management of sepsis in a 51-year-old woman with stage IIIA HER2-positive breast cancer who developed eroded mixed hemorrhoids during neoadjuvant TCHP chemotherapy (docetaxel, carboplatin, trastuzumab, pertuzumab). Conservative multimodal treatment was used because severe chemotherapy-induced neutropenia and septicemia made standard surgery high risk, and the approach was successful. The report highlights a clinically significant alternative pathway for treating anorectal complications during intensive breast cancer chemotherapy when operative management is dangerous.

Ye Z, Xie H, Lan X et al. · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Critical Kennedy’s disease with Guillain-Barré syndrome and respiratory failure: A case report.

This case report examined critical care management of a 61-year-old man with spinal and bulbar muscular atrophy (Kennedy disease, SBMA) who developed Guillain-Barré syndrome with respiratory failure. The key finding was that acute decompensation in SBMA can be complicated by a superimposed immune-mediated neuropathy (Guillain-Barré syndrome), requiring ICU-level respiratory support and attention to treatable causes. Clinically, it underscores the importance of evaluating for immune-mediated neuropathies in SBMA patients presenting with respiratory failure rather than attributing deterioration solely to neurodegeneration.

Gao X, Yu K · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

ESBL-Producing Klebsiella pneumoniae Bacteraemia with Renal Micro-Abscesses Treated with Cefepime-Enmetazobactam in a Neutropenic Allogeneic Transplant Recipient.

This case report studied treatment of ESBL-producing Klebsiella pneumoniae bacteremia with renal micro-abscesses in a profoundly immunocompromised adult with acute myeloid leukemia after allogeneic hematopoietic stem cell transplantation (allo-HSCT) and neutropenia. The patient was treated with cefepime–enmetazobactam and the infection involving renal micro-abscesses was managed successfully despite the patient’s high risk for difficult-to-treat ESBL bloodstream infection. The report supports cefepime–enmetazobactam as a potential carbapenem-sparing option in severe ESBL Enterobacterales infections in post-transplant neutropenic patients, where carbapenem exposure may worsen dysbiosis and drive resistance.

Tascini C, Montanari L, Patriarca F et al. · Pathogens (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

---

Viral Immunology, Vaccines & Antiviral Mechanisms

NS1-Induced PARP1 Phase Transitions Prolongs Host Transcriptional Pausing to Promote Influenza A Virus Replication.

The study investigated how influenza A virus (IAV) nonstructural protein NS1 manipulates host PARP1 to control viral replication by combining CRISPR screening, ATAC-seq, and biophysical/condensate analyses. NS1 binding to PARP1’s helical domain drove PARP1 phase transitions that trapped RNA polymerase II in prolonged promoter-proximal transcriptional pausing by enriching pausing factors such as SPT5-PLD, promoting IAV replication. This mechanistic link between NS1–PARP1 condensates and host transcriptional pausing identifies PARP1 phase behavior as a potential antiviral intervention point.

Ma S, Kang C, Liu X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Epstein-Barr virus gp350 neutralizing epitopes define distinct sites of vulnerability.

This study mapped Epstein-Barr virus (EBV) gp350 neutralizing epitopes using human monoclonal antibodies isolated from a phage-display library derived from EBV-seropositive donors and evaluated protection in a humanized mouse model. A lead antibody, 1A12, defined a vulnerable gp350 site and conferred robust protection by markedly reducing viral load and disease pathology, while structural epitope mapping identified three distinct antigenic vulnerability sites. These findings advance EBV vaccine design by pinpointing actionable neutralizing epitope targets on gp350.

Zhao GX, Li PL, Yuan BY et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Epstein-Barr Virus: More than Just an Infection.

This narrative review analyzed how Epstein-Barr virus (EBV) contributes to immunopathological diseases, focusing on viral latency/lytic switching and the role of EBNA1. It found that EBNA1 can drive autoimmunity via molecular mimicry (including GlialCAM in multiple sclerosis, keratin in rheumatoid arthritis, and nuclear proteins in systemic lupus erythematosus) and that bystander activation and epitope spreading amplify disease. Scientifically, it frames EBV as more than an infection by linking specific EBV programs and proteins to mechanisms of autoimmunity across multiple disorders.

Van de Perre E, Van Nieuwenhuyse B, Yombi JC · Viruses · (2026) · View on PubMed ↗ · Free PDF ↗

---

Respiratory Virus Epidemiology & Forecasting

Seasonal and Age-Stratified Patterns of Influenza, COVID-19, and RSV in Poland (2024-2026).

This study analyzed nationwide Polish surveillance data (2024/25 and 2025/26) to characterize seasonal and age-stratified patterns of influenza, COVID-19, and RSV across age groups (0–4, 5–19, 20–59, ≥60 years). The key finding was that the three respiratory viruses showed similar seasonal circulation dynamics with comparable peak timing/width and measurable age-specific lead–lag relationships between viruses. This is significant for public health planning because it supports more coordinated, age-targeted forecasting and intervention timing for concurrent respiratory epidemics.

Majewska W, Poniedziałek B, Brydak LB et al. · Viruses · (2026) · View on PubMed ↗ · Free PDF ↗

---

Obesity, Oxidative Stress & Metabolic Inflammation

Nucleotide metabolic reprogramming: a “double-edged sword” in obesity-related inflammation-from metabolic adaptation to pathological imbalance.

This article (a mechanistic review) discusses how nucleotide metabolic reprogramming can drive obesity-related inflammation via a “double-edged sword,” focusing on reduced NLRP3 inflammasome activation threshold and mitochondrial DNA/oxidative damage. It highlights a pathway in which obesity-induced phosphorylation and inactivation of SAMHD1 leads to cytosolic dNTP accumulation, increased mitochondrial dNTP entry via PNC1/2 transporters, uncontrolled mtDNA synthesis, and consequent oxidative damage that promotes excessive NLRP3 activation. The scientific significance is that it consolidates a causal metabolic-to-inflammasome axis that could be targeted to treat obesity-associated sterile inflammation.

Li Z, Liu Y, Ouyang X et al. · Journal of physiology and biochemistry · (2026) · View on PubMed ↗ · Free PDF ↗

Factors associated with sarcopenia in elderly patients with type 2 diabetes mellitus.

This systematic review and meta-analysis aimed to identify factors associated with sarcopenia in older adults with type 2 diabetes mellitus by synthesizing age-specific evidence. The key output is a quantitative summary of which clinical factors show statistically supported associations with sarcopenia in this older T2DM population. Clinically, it helps clinicians target modifiable risks and refine screening for sarcopenia among older patients with type 2 diabetes.

Cao Z, Li J, Gao X et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

Oxidative Stress as a Pathophysiological Core of Obesity: Preclinical Evidence for Antioxidant-Based Therapy Strategies.

This preclinical evidence review synthesized research on obesity as a redox/oxidative-stress disorder and evaluated antioxidant-based therapeutic strategies. It found that visceral adipose expansion impairs antioxidant defenses (e.g., superoxide dismutase, catalase, glutathione peroxidase) and sustains chronic low-grade inflammation through NF-κB and NADPH oxidase pathways, providing mechanistic rationale for antioxidant interventions. The scientific significance is that targeting oxidative stress may represent a complementary therapeutic approach to obesity beyond calorie/energy balance.

Pereira MM, Amorim CS, Gomes ACCA et al. · Pharmaceuticals (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of Curcumin in Neurodegenerative Diseases: From Pharmacokinetic Barriers to Advanced Delivery Systems.

This review assessed curcumin’s therapeutic potential for neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and ALS) with emphasis on pharmacokinetic barriers and advanced delivery systems. The key finding was that curcumin’s poor oral bioavailability (<1%) and negligible blood–brain barrier penetration (<0.1%) have limited clinical translation, but newer delivery approaches are being developed to overcome these constraints. Clinically, it supports continued optimization of curcumin formulations as a strategy to improve brain exposure and enable more effective testing in neurodegenerative disease.

Castello-Guillen A, Garrido-Reig M, Caplliure-Llopis J et al. · Pharmaceuticals (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

Foods as Modulators of GLP-1 Secretion.

This narrative review summarized evidence that dietary components can modulate endogenous GLP-1 secretion from enteroendocrine L-cells. The key finding was that specific food matrices and gut microbiota-dependent pathways can increase GLP-1 release, although the physiological magnitude is generally modest compared with pharmacologic GLP-1 receptor agonists. This is significant for nutrition-based strategies aiming to improve metabolic health by enhancing incretin signaling through diet.

Tkaczenko H, Kołodziejska R, Rymuszka A et al. · Nutrients · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists and Tirzepatide in Men Seeking Fertility: A Structured Narrative Review and Proposed Clinical Framework.

This structured narrative review examined evidence on GLP-1 receptor agonists (e.g., liraglutide/semaglutide) and the dual GIP/GLP-1 agonist tirzepatide in men seeking fertility, focusing on endocrine, semen, sexual-function, and clinical fertility outcomes. Across available studies, total testosterone tended to increase in metabolically impaired men, while effects on free testosterone and gonadotropin suppression were inconsistent and short-term studies did not show the degree of gonadotropin suppression expected from the mechanism. The proposed clinical framework is intended to guide counseling of reproductive-age men about potential reproductive and hormonal implications when using GLP-1–based therapies.

Kaltsas A, Gkioxaris V, Giannakas T et al. · Journal of clinical medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Skeletal Muscle Effects of GLP 1 Receptor Agonists: Molecular Mechanisms and Comparative Insights on Semaglutide and Tirzepatide, a Narrative Review.

This narrative review studied skeletal muscle effects of GLP-1 receptor agonists and related incretin therapies, comparing mechanistic insights for semaglutide versus tirzepatide. It highlights that while these drugs reduce body weight, a substantial portion of weight loss can come from decreased lean mass, raising concern for sarcopenia risk—especially in older or frail individuals—though sarcopenia requires deficits in muscle mass plus strength and physical function. The significance is that clinicians should monitor not only weight but also lean mass and functional outcomes when using GLP-1–based therapies, particularly in high-risk populations.

Cautela D, Incarbona V, Lombardi A et al. · International journal of molecular sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Genome-wide mapping of common and rare variant effects on adiposity across childhood.

This genome-wide study mapped common and rare variant effects on adiposity across childhood using age-stratified genetic association analyses in large cohorts with objectively measured childhood adiposity (n=62,276) and recalled childhood adiposity traits (n=599,924). It found 624 common variants associated with childhood adiposity and identified childhood-specific effects in pathways including the leptin–melanocortin axis (BSX, GNAS, LEPR, PCSK1) and incretin signaling (GIPR, GLP1R), with one-third of signals not concordant with adult BMI. The significance is that it refines the genetic architecture of obesity by highlighting childhood-specific biology that could inform age-tailored risk prediction and interventions.

Kentistou KA, Sundfjord J, Karimi R et al. · Nature genetics · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neurodegeneration, Neuroinflammation & Biomarkers

14-3-3γ Protects Against Postoperative Cognitive Dysfunction by Regulating Tau Thr205 Phosphorylation and Synaptic Integrity.

The study assessed whether 14-3-3γ protects against postoperative cognitive dysfunction (POCD) by analyzing CSF proteomic biomarkers in the ADNI cohort (SomaScan 7K; n=237) and measuring circulating 14-3-3γ in a prospective surgical cohort (n=213), followed by mechanistic testing in mice. It found that 14-3-3γ modulates tau Thr205 phosphorylation and preserves synaptic integrity, thereby reducing POCD-like outcomes in the surgical model using AAV-mediated gene manipulation, neuronal culture, pharmacology, and molecular dynamics simulations. This positions 14-3-3γ–tau signaling as a candidate biomarker and therapeutic axis for preventing cognitive decline after surgery.

Zhu S, Han X, Zhang H et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

PLXDC2 siRNA-Mediated Intervention Attenuates Microglial Senescence Through cGAS-STING Signaling.

This study tested whether PLXDC2 knockdown using PLXDC2 siRNA can attenuate microglial senescence through cGAS–STING signaling in Parkinson’s disease (PD) models, guided by a human substantia nigra single-cell atlas. PLXDC2 was upregulated in PD microglia, and a BBB-penetrating biomimetic nanoplatform (HFn-GM@siPLXDC2/DFO/CeO2-NP) delivering PLXDC2-targeting siRNA together with deferoxamine (iron chelation) and CeO2 (antioxidant) suppressed cGAS–STING–linked senescence phenotypes in vivo. The approach links a specific microglial target (PLXDC2) to innate immune activation (cGAS–STING) and suggests a combinatorial nanotherapy strategy for PD-related neuroinflammation and iron/oxidative stress.

Lu H, Zheng Z, Wang F et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Alzheimer’s Disease: From Molecular Pathogenesis to Disease-Modifying Therapies and Clinical Implementation in Aging Populations.

This narrative review summarized molecular pathogenesis and disease-modifying therapy development for Alzheimer’s disease (AD), with emphasis on clinical implementation in aging populations. It highlighted that anti-amyloid monoclonal antibodies lecanemab (2023) and donanemab (2024) modestly but significantly slow clinical decline by targeting amyloid-β pathology compared with earlier symptomatic treatments (cholinesterase inhibitors and memantine). The review’s significance is translating emerging amyloid-targeting evidence into practical, population-aware clinical decision-making for AD care.

Zrineh A, Akwan R, Darawsheh R et al. · Clinical interventions in aging · (2026) · View on PubMed ↗ · Free PDF ↗

The Versatile Roles of Exosomes in Neurodegenerative Disorders: From Pathological Mechanism and Diagnostic Biomarkers to Therapeutic Application.

This review article summarized the roles of exosomes in neurodegenerative disorders, covering pathological mechanisms, diagnostic biomarker potential, and therapeutic applications. It described how exosomes (30–150 nm extracellular vesicles) mediate intercellular transport of biomolecules and influence processes such as signal transduction and immune modulation across neurodegenerative contexts. The scientific significance is consolidating current evidence to guide development of exosome-based diagnostics and therapies for diseases that currently lack cures.

Liu R, Yue H, Li X et al. · Drug design, development and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Lithium chloride in vitro treatment shows potential to rescue the neuronal phenotype caused by WDFY3 haploinsufficiency.

This study characterized loss-of-function (LoF) variants in WDFY3 in a cohort of 32 individuals and tested WDFY3 haploinsufficiency mechanisms using knockdown in SH-SY5Y human neuroblastoma cells and a Wdfy3-haploinsufficient mouse model. WDFY3 LoF impaired clearance of protein aggregates and reduced p62 (SQSTM1) protein levels, consistent with disrupted ubiquitin-dependent proteostasis. These findings support a mechanistic basis for WDFY3-associated neuropsychiatric/neurodevelopmental disorder and motivate lithium chloride as a potential in vitro rescue strategy.

Paha MJ, Mustafa A, Tat L et al. · Molecular psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Activation of TREM2 via single-domain antibodies improves synaptic and cognitive function in 5×FAD mice.

This study tested whether activating triggering receptor expressed on myeloid cells 2 (TREM2) using two TREM2-activating single-domain antibodies (sdAbs), 10C11 and 10E12, improves synaptic and cognitive outcomes in early-stage 5×FAD transgenic mice after ventral hippocampal injection. The key finding was that both sdAbs activated microglia and rescued cognitive deficits, with 10E12 reducing Aβ plaque burden (and associated pathology) in this Alzheimer’s disease model. Scientifically, it supports TREM2 activation as a therapeutic mechanism and provides antibody-based evidence linking microglial TREM2 signaling to reduced amyloid pathology and improved cognition.

Yu X, Ren Q, Gao Y et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Insights into X-linked Dystonia-Parkinsonism and Spinocerebellar Ataxia type 36 Through the Lens of Amyotrophic Lateral Sclerosis/Frontotemporal Dementia.

This article reviewed insights into X-linked dystonia-parkinsonism (XDP) and spinocerebellar ataxia type 36 (SCA36) by comparing them with amyotrophic lateral sclerosis/frontotemporal dementia (ALS/FTD) caused by C9orf72 repeat expansions. The key finding is that these hexanucleotide repeat disorders share expanded intronic repeat architecture capable of forming non-canonical nucleic acid structures but diverge in critical molecular mechanisms (e.g., TDP-43 aggregation in C9orf72-ALS/FTD). The significance is a framework for understanding how RNA toxicity and protein toxicity pathways differ across repeat-expansion diseases, guiding more targeted mechanistic and therapeutic strategies.

Patel M, Das S, Kumari AP et al. · Molecular neurobiology · (2026) · View on PubMed ↗

Neuroinflammation and metabolic reprogramming in Parkinson’s disease.

This Frontiers in Immunology review synthesized current evidence on neuroinflammation and metabolic reprogramming as intertwined mechanisms in Parkinson’s disease (PD), centered on α-synuclein (αSyn) pathology and degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The key integrative proposition is a mechanistic model in which inflammatory signaling and metabolic dysfunction mutually reinforce PD initiation and progression. Scientifically, it frames potential disease-modifying strategies that target both immune pathways and metabolic circuits rather than treating neuroinflammation or metabolism in isolation.

Fu Y, Yu J, Xu L et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Real-world implementation of lecanemab in Alzheimer’s disease: A Japanese cohort.

This Japanese real-world cohort study evaluated lecanemab implementation in early Alzheimer’s disease (AD) by screening 321 patients with confirmed amyloid pathology using amyloid PET or cerebrospinal fluid analysis. Among 102 lecanemab initiators, structured MRI surveillance over 6 months was used to assess feasibility, safety, biomarker profiles (including plasma amyloid-β42/40 when available), and short-term clinical outcomes. The findings provide practical evidence on how lecanemab performs in routine care in an Asian population, informing monitoring and expectations for safety and biomarker response.

Shimohama S, Bun S, Shikimoto R et al. · Alzheimer’s & dementia (Amsterdam, Netherlands) · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative efficacy of neuromodulation techniques for Alzheimer’s disease: a systematic review and network meta-analysis of randomized controlled trials.

This systematic review and network meta-analysis compared neuromodulation techniques (NMTs) for Alzheimer’s disease across randomized controlled trials, ranking effects on cognitive, activities of daily living (ADLs), and neuropsychiatric outcomes. The key finding was that different NMT modalities showed differential efficacy profiles across these domains, enabling comparative ranking rather than relying on single-trial results. Clinically, it helps guide selection of the most beneficial neuromodulation approach for AD patients based on outcome-specific evidence.

Liu Y, Liu S, Yan H et al. · Frontiers in neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗

Serum GFAP and Age Accurately Distinguish AQP4-IgG Positive and Double Seronegative NMOSD From MOGAD After a Recent Attack.

This cohort study measured serum neurofilament-light chain (sNfL) and glial fibrillary acidic protein (sGFAP) in 640 patients from the OFSEP cohort to distinguish AQP4-IgG positive NMOSD and double-seronegative NMOSD from MOGAD after a recent attack. The key finding was that serum GFAP (sGFAP), together with age, accurately discriminated these NMOSD subtypes from MOGAD in the post-attack setting. This has diagnostic significance by improving biomarker-based differentiation of NMOSD versus MOGAD, which can guide appropriate treatment selection.

Rival M, Rollot F, Laurent-Chabalier S et al. · European journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Advanced Eye Movement Features Measured by Quantitative Oculography as Candidate Biomarkers for Progressive Supranuclear Palsy.

This review studied quantitative eye-movement biomarkers in progressive supranuclear palsy (PSP), focusing on video-oculography (VOG) metrics from advanced saccade tasks (prosaccades, antisaccades, memory-guided, predictive, overlap, and gap saccades) across PSP populations and comparisons with other neurodegenerative diseases. It found that subtle, task-specific oculomotor abnormalities measurable by VOG can distinguish PSP subtypes and help differentiate PSP from other disorders that may be missed by qualitative bedside testing. These findings support quantitative oculography as a clinically useful, objective tool for earlier and more accurate PSP diagnosis and stratification.

Ouyang H, Liu B, Peng Q et al. · Diagnostics (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neuroimmune & Mast Cell Biology

Cannabinoid CB1 Receptor in Nociceptors Mediates Postoperative Analgesia via ASIC3 Inhibition.

The study examined how cannabinoid type-1 receptor (CB1R), specifically in nociceptors/primary sensory neurons, regulates postoperative pain in a mouse plantar-incision model using nociceptor-selective Cnr1 knockout and site-specific pharmacology. CB1R activation alleviated postoperative mechanical allodynia by colocalizing and physically associating with the proton-sensing ion channel ASIC3, thereby inhibiting ASIC3 activity in CGRP+ peptidergic nociceptors. These findings support peripheral CB1R–ASIC3 pathway targeting as a mechanistic strategy for analgesia with reduced central side effects after surgery.

Xu K, Ji L, Yang H et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Epidermal HLA-DQB1 exerts negative regulation of mast cell activation through the TSLP-driven SPP1-expressing macrophage axis.

This mechanistic immunology study investigated how epidermal HLA-DQB1 regulates mast cell activation in IgE-mediated skin inflammation, integrating Mendelian randomization, immunohistochemistry, and a keratinocyte-specific H2-Ab1 knockout mouse model (K14Cre/+H2-Ab1fl/f). The authors found that epidermal MHC-II (HLA-DQB1/H2-Ab1 axis) negatively regulates mast cell activation through a TSLP-driven SPP1-expressing macrophage axis. These results identify a keratinocyte–macrophage–mast cell regulatory pathway that could be targeted for urticaria and related inflammatory skin diseases.

Yi X, Shui X, Zheng Q et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

Mast Cells in Neuroimmune Interactions: Mechanisms, Pathophysiological Roles, and Therapeutic Implications.

This review summarizes the roles of mast cells (MCs) in neuroimmune interactions across central nervous system and peripheral barrier tissues and discusses therapeutic implications. The key finding is that MCs can rapidly release mediators such as histamine, tryptase, TNF-α, IL-1β, substance P, and prostaglandins that modulate nerve signaling, vascular function, and inflammation. Scientifically and clinically, it provides an integrated mechanistic basis for considering MCs as therapeutic targets in neuroinflammatory and neurodegenerative conditions.

Hasan A, Asfour AAR, Qaba H et al. · Molecular neurobiology · (2026) · View on PubMed ↗

---

Autoimmunity & Infectious Triggers (Causality Frameworks)

Nutrition and Endometriosis: Current Evidence on Dietary Risk Factors and Clinical Impact - A Narrative Review.

This narrative review evaluated evidence linking nutrition and dietary risk factors to endometriosis and discussed clinical impacts. It emphasized that approximately 10% of women of reproductive age are affected, that current treatments (hormonal therapy, surgery, pain management) have limitations, and that nutrients/phytochemicals may modulate inflammation, oxidative stress, immune function, and hormonal balance. Clinically, it supports dietary strategies as potential adjuncts for endometriosis-associated pain and disease management while highlighting the need for stronger evidence.

Dawczynski C, Raschke J, Klein L et al. · Journal of inflammation research · (2026) · View on PubMed ↗ · Free PDF ↗

Infectious triggers in IgA vasculitis in children: current evidence, causal attribution and immunopathogenic mechanisms.

This review evaluated infectious triggers in pediatric IgA vasculitis (IgAV) by distinguishing epidemiological associations from incidental detections and infectious mimics, and by separating direct IgAV evidence from extrapolated mechanisms from IgA nephropathy and mucosal immunology. The key finding is that temporally proximate microbiological detection alone is insufficient for individual-level causality, and the evidence base must be interpreted through rigorous causal attribution frameworks. Clinically, it clarifies what current evidence supports regarding infection-driven IgAV onset and helps guide future studies aimed at identifying true causal pathogens and mechanisms.

Filippatos F, Venieri D, Tsigkrou E et al. · Rheumatology international · (2026) · View on PubMed ↗ · Free PDF ↗

Associations Between Early-Life Exposure to Different Antibiotic Agents and the Risks of Autism Spectrum Disorder and Attention-Deficit/Hyperactivity Disorder: A Nationwide Population-Based Study.

This nationwide population-based case-control study evaluated whether early-life exposure to different antibiotic agents is associated with later autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) in Taiwan. The key finding was that antibiotic exposure in infancy showed differential associations with ASD and ADHD risk depending on the specific antibiotic agents used (with outcomes assessed through 2022 follow-up). This is significant because it suggests that not all early antibiotic exposures carry the same neurodevelopmental risk profile, informing more tailored antibiotic stewardship.

Lee HY, Chang YC, Chen CL et al. · Pharmaceutics · (2026) · View on PubMed ↗ · Free PDF ↗

Association Between Toe Walking and Repetitive Behaviors in Children with Autism Spectrum Disorder: A Cross-Sectional Phenotypic Analysis.

This cross-sectional phenotypic analysis studied toe walking in 289 children with autism spectrum disorder (ASD) and its association with repetitive behaviors using comprehensive clinical assessments. Toe walking showed a relationship with the ASD behavioral phenotype, particularly with measures of repetitive behaviors (as evaluated alongside motor, sleep, and feeding behavior scales). Clinically, identifying toe walking as a marker linked to repetitive behavior profiles could help refine behavioral characterization and target interventions in children with ASD.

Gnazzo M, Bargiacchi G, Gallai B et al. · Medicina (Kaunas, Lithuania) · (2026) · View on PubMed ↗ · Free PDF ↗

Optimizing the Endometrial Factor in Recurrent Implantation Failure: From Established Diagnostics to Mechanism-Informed Management.

This narrative review studied recurrent implantation failure (RIF) in the context of assisted reproductive technology by synthesizing evidence on endometrial receptivity diagnostics and mechanism-informed management. It highlights that endometrial factors—rather than embryo quality alone—contribute to a substantial fraction of otherwise unexplained RIF, and it summarizes current diagnostic approaches and therapeutic strategies targeting specific endometrial mechanisms. The review’s significance is to provide a practical, mechanism-based roadmap for clinicians to evaluate and treat endometrial contributors to RIF.

Zikopoulos A, Moustakli E, Potiris A et al. · Journal of clinical medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Molecular histomorphometry and the emerging role of transcriptomics in celiac disease diagnosis and therapeutic trials.

This review studied how molecular histomorphometry and transcriptomic profiling can improve celiac disease (CeD) diagnosis and monitoring compared with conventional serology and small-intestinal histology. It found that transcriptomic technologies can reveal disease-specific intestinal mucosal gene-expression signatures and that more quantitative histomorphometric approaches may detect subtle mucosal changes with less interobserver variability, particularly in treated or early disease. The significance is that these molecular tools could enable more accurate diagnosis, better disease monitoring, and more informative therapeutic trial endpoints in CeD.

Viiri K, Chongtham C, Mäki M · Annals of medicine · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cardiovascular Risk, Lipids & Real-World Treatment Effectiveness

Salvianolic Acid a Disrupts the HSP90α-AKT-PERK Ternary Complex to Alleviate Atherosclerosis by Activating Endoplasmic Reticulum Stress of Senescent Vascular Smooth Muscle Cells.

The study evaluated whether salvianolic acid A (SAA) can target senescent vascular smooth muscle cells (VSMCs) to alleviate atherosclerosis, using senescent VSMC models with HSP90α overexpression/knockdown and ApoE-/- high-fat diet mice with AAV-mediated VSMC-specific HSP90α manipulation. SAA promoted apoptosis in senescent VSMCs by inhibiting HSP90α and disrupting the HSP90α–AKT–PERK ternary complex, thereby activating endoplasmic reticulum stress. This mechanistic targeting of HSP90α–AKT–PERK signaling by SAA highlights a potential therapeutic approach for reducing atherosclerosis driven by VSMC senescence.

Guan X, Lu M, Cui X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Extracellular Vesicle Packaged TDP43 Derived From ECs Exacerbates Cigarette Tar-Related Atherosclerosis Progression via Enhancing Macrophage Extracellular Traps.

This study investigated whether extracellular vesicles (EVs) carrying TDP43 from cigarette tar (TAR)-treated endothelial cells exacerbate atherosclerosis in TAR-injected ApoE-/- mice and in macrophage co-culture systems. TAR increased endothelial EV secretion and worsened plaque burden, while EV inhibition with GW4869 reduced lesions, and transcriptomic analyses linked TAR-driven progression to enhanced macrophage extracellular trap (MET) formation. The work supports a smoking–EV–TDP43–MET axis as a potential therapeutic target to slow TAR-related atherosclerosis progression.

Zhu X, Chen Y, Meng W et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Ilexoside K Ameliorates Atherosclerosis by Suppressing CD72hi Macrophages and Blocking CXCL12-CXCR4 Axis to Inhibit Endothelial Pyroptosis.

This study examined the role of a c-Rel–driven CD72hi macrophage subset in atherosclerosis and tested whether the natural triterpenoid saponin Ilexoside K (IK) can block the downstream mechanism in human and murine plaque models. Single-cell transcriptomics and functional assays showed CD72hi macrophages promote endothelial pyroptosis via pathological crosstalk through the CXCL12–CXCR4 axis, and transcriptome-based screening identified IK as a dual anti-atherosclerotic and anti-pyroptotic agent. These results support targeting the CD72hi macrophage–CXCL12/CXCR4–pyroptosis pathway as a strategy to reduce residual inflammatory risk in ASCVD.

He X, Li S, Chen J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Multi-target blood test for hepatocellular carcinoma early detection: a cross-sectional analysis of the prospective ALTUS study.

In the prospective, multicenter ALTUS study, adults with cirrhosis or chronic HBV infection eligible for routine HCC screening were evaluated in a head-to-head comparison of the multi-target HCC blood test (mt-HBT) versus standard ultrasound. The key finding was that mt-HBT demonstrated non-inferior sensitivity for early-stage HCC compared with ultrasound while also assessing specificity (details truncated in the abstract). If confirmed, mt-HBT could improve early HCC detection where ultrasound sensitivity and screening adherence are limited.

John BV, Camardo M, Singal AG et al. · Journal of hepatology · (2026) · View on PubMed ↗

Risk factors of primary angle-closure glaucoma: An exposome-wide association study in the China Kadoorie Biobank.

Using the China Kadoorie Biobank (n=499,102; ages 30–79), this exposome-wide association study assessed systemic metabolic, vascular, and lifestyle exposures for incident probable primary angle-closure glaucoma (prob PACG) over a median 15.7-year follow-up. The analysis applied elastic-net, XGBoost, and Cox regression to identify exposures associated with prob PACG incidence (specific exposures truncated in the abstract). These findings broaden PACG risk beyond ocular anatomy and support prevention strategies targeting modifiable systemic factors.

Shao Z, Gong S, Li C et al. · Asia-Pacific journal of ophthalmology (Philadelphia, Pa.) · (2026) · View on PubMed ↗ · Free PDF ↗

Independent and joint predictive value of Lipid Accumulation Product and estimated Pulse Wave Velocity for incident depressive symptoms: Evidence from CHARLS.

In CHARLS (2011–2020), the study examined whether Lipid Accumulation Product (LAP) and estimated pulse wave velocity (ePWV) predict incident depressive symptoms among 5,216 Chinese adults. The key finding was that metabolic dysfunction (LAP) and vascular aging/arterial stiffness (ePWV) showed independent and joint predictive associations with later depressive symptoms. This supports a vascular-metabolic pathway for depression risk stratification in population settings.

Sun Y, Zhao Z, Sun Y et al. · Journal of affective disorders · (2026) · View on PubMed ↗

Efficacy and Safety of ACEi, ARB, and ARNi in Cardiac Amyloidosis: A Retrospective Propensity Score-Matched Cohort Study.

Using the TriNetX Research Network, this retrospective propensity score–matched cohort study compared ACE inhibitors (ACEi), ARBs, and ARNi versus no use in patients with cardiac amyloidosis, with outcomes tracked for up to 3 years. After 1:1 propensity score matching, the study assessed all-cause mortality and safety events including hypotension, acute kidney injury, hyperkalemia, dizziness, and hospitalization (subgroup details truncated). The findings clarify comparative effectiveness and tolerability of RAAS/ARNI strategies in cardiac amyloidosis, where evidence is less established than in other heart failure phenotypes.

Kawtharany H, Mahmoud N, Rayyan A et al. · Current problems in cardiology · (2026) · View on PubMed ↗

Balance of non-Lp(a) apoB and Lp(a) with Coronary Plaque Phenotypes and MACE: Insights from PROSPECT II and CASABLANCA.

This study assessed associations between non–Lp(a) apoB, Lp(a), and their relative balance with coronary plaque phenotypes and major adverse cardiovascular events (MACE) in 854 patients with recent myocardial infarction from the PROSPECT II NIRS-IVUS cohort. The key finding was that the non–Lp(a) apoB/Lp(a) ratio (derived from apoB conversion to nmol/L and subtraction of Lp(a)) related to plaque burden and vulnerability, linking lipoprotein composition balance to subsequent clinical risk. Clinically, this supports using combined apoB and Lp(a balance metrics—beyond either marker alone—to refine risk stratification after MI.

Tsimikas S, Januzzi JL, Maeng M et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗ · Free PDF ↗

Simulation-based dosimetric analysis of surgeon radiation exposure during robotic-assisted versus conventional URS.

This simulation-based dosimetric study compared surgeon radiation exposure during robotic-assisted versus conventional ureteroscopy (URS) by modeling fluoroscopy time and estimating doses at multiple positions using retrospective fluoroscopy data from 35 clinical cases. The key finding was that a three-stage simulation approach using robotic-assisted and non-robotic-assisted phases could quantify differences in estimated surgeon exposure between the two URS modalities. The clinical significance is improved occupational radiation safety assessment for surgical teams and evidence to support robotic systems as potentially safer alternatives during URS.

Ergül RB, İnceoğlu ŞN, Özdemir B et al. · World journal of urology · (2026) · View on PubMed ↗

Cardiotoxicity of macrolide antibiotics: a pharmacovigilance study integrating FAERS and JADER databases.

This pharmacovigilance study analyzed macrolide-associated cardiac adverse events (cAEs) in real-world drug safety reports from the FDA Adverse Event Reporting System (FAERS) and the Japanese Adverse Drug Event Report database (JADE). Disproportionality analyses identified drug-specific signal patterns for cardiotoxicity (including QT-prolongation–related cardiac events) and characterized associated clinical outcomes across the two national datasets. These cross-national, large-scale safety signals can inform clinicians and regulators about which macrolide antibiotics may carry higher cardiotoxic risk and guide monitoring and risk mitigation.

Zhou L, Zhou Y, Liu C et al. · Naunyn-Schmiedeberg’s archives of pharmacology · (2026) · View on PubMed ↗

Occurrence of progressive pulmonary fibrosis and its association with survival in connective tissue disease-associated interstitial lung disease: an international retrospective cohort study.

This international retrospective cohort study evaluated adults with connective tissue disease-associated interstitial lung disease (CTD-ILD) due to rheumatoid arthritis, systemic sclerosis, mixed connective tissue disease, and other CTDs, and assessed when progressive pulmonary fibrosis (PPF) began using INBUILD and/or ATS/ERS/JRS/ALAT criteria applied in routine care. PPF onset was analyzed with time-to-event methods to determine associations with survival and other clinical outcomes in 357 patients. The findings support real-world identification of PPF in CTD-ILD and may help clinicians stratify prognosis and target earlier interventions.

Guiot J, Teitsma XM, Dimitroulas T et al. · Rheumatology international · (2026) · View on PubMed ↗

Menopause Hormone Therapy in Women With Cardiovascular Risk Factors or Established Ischemic Heart Disease: A Joint FIGO and WHF Position Paper.

This FIGO and World Heart Federation (WHF) joint position paper reviewed evidence on systemic menopause hormone therapy (MHT) in women with cardiovascular risk factors or established ischemic heart disease. The key conclusion is that starting systemic MHT early—ideally soon after symptom onset and within 10 years of the final menstrual period—can alleviate climacteric symptoms and is associated with long-term cardiovascular benefits in appropriately selected patients. Clinically, it provides guidance for balancing symptom control with cardiovascular risk when considering MHT in higher-risk women.

Benedetto C, Gulati M, Khadilkar SS et al. · Global heart · (2026) · View on PubMed ↗ · Free PDF ↗

Longitudinal Trajectories of Body Roundness Index and Risk of Incident Hypertension in Non-Diabetic Elderly Adults: A Prospective Nationwide Cohort Study Involving Two Cohorts.

This prospective nationwide cohort study assessed longitudinal trajectories of body roundness index (BRI) and their association with incident hypertension in non-diabetic older adults using the China Health and Retirement Longitudinal Study (CHARLS) with external validation in the English Longitudinal Study of Ageing (ELSA). The analysis used repeated BRI measurements across waves (2011–2016) to model trajectories and relate them to time-to-event development of hypertension. The results support using trajectory-based central adiposity metrics rather than single measurements to better predict hypertension risk in non-diabetic aging populations.

Gao X, Liu Y, Xiong B et al. · Global heart · (2026) · View on PubMed ↗ · Free PDF ↗

Independent and joint effects of lifestyle, human leukocyte antigen polymorphisms on cancer risk: findings from the UK Biobank.

This UK Biobank study assessed independent and joint effects of a healthy lifestyle index (diet, smoking, alcohol, physical activity, adiposity) and imputed classical HLA polymorphisms (50 alleles across 11 HLA genes) on overall and site-specific cancer risk in 159,744 men and 175,037 women of European ancestry. The key finding was that both lifestyle and specific HLA alleles contributed to cancer susceptibility and that their effects could act jointly in sex-stratified analyses. These results support integrating immune-genetic risk (classical HLA variation) with modifiable lifestyle factors to improve cancer risk stratification and prevention strategies.

Zheng J, Jiang S, Zhu H et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

The 2026 ACC/AHA Dyslipidemia Guideline: A Critical and Transatlantic Perspective on Personalized Lipid Management.

This critical review studied the 2026 ACC/AHA dyslipidemia guideline and its implications for personalized lipid management, emphasizing how recommendations extend beyond LDL-C to include non-HDL-C, ApoB, lipoprotein(a), triglyceride-rich lipoproteins, inherited lipid disorders, and severe hypertriglyceridemia. The key finding is that the guideline introduces structured risk-enhancer integration, renewed explicit lipid targets, and PREVENT-ASCVD to support more individualized cardiovascular prevention strategies. Clinically, it helps clinicians interpret which recommendations are outcome-evidence–supported versus those based on other considerations when tailoring lipid-lowering therapy.

Sabouret P, Mafrica D, Giamundo DM et al. · Life (Basel, Switzerland) · (2026) · View on PubMed ↗ · Free PDF ↗

Features of Lipid Disorders in Cardiovascular-Kidney-Metabolic Syndrome.

This review studied lipid disorder patterns in cardiovascular-kidney-metabolic (CKM) syndrome, describing the characteristic dyslipidemic phenotype driven by visceral adiposity, insulin resistance, inflammation, oxidative stress, and kidney dysfunction. It finds that CKM syndrome is associated with elevated triglycerides, reduced HDL-C, increased apoB-containing lipoproteins, remnant cholesterol accumulation, small dense LDL particles, and often elevated lipoprotein(a) (Lp(a)). The clinical significance is that recognizing this lipid signature may help target therapies to reduce accelerated atherosclerosis and early renal deterioration in CKM patients.

Ceasovschih A, Şener YZ, Arici M et al. · International journal of molecular sciences · (2026) · View on PubMed ↗ · Free PDF ↗

The Heart-Kidney Axis in Heart Failure and Chronic Kidney Disease: Mechanisms, Mediators, and Therapeutic Implications.

This review studied the heart–kidney axis in heart failure and chronic kidney disease, synthesizing mechanisms and mediators (hemodynamic/neurohormonal plus endocrine, inflammatory, and metabolic pathways) that drive cardiorenal syndrome and cardiovascular–kidney–metabolic disease. It found that cross-organ injury is coordinated by multiple non-hemodynamic mediators, implying that disruption of the axis is not solely explained by blood-pressure or neurohormonal changes. The work is significant because it frames therapeutic implications for targeting these shared mediators to improve outcomes in cardiorenal syndrome.

Fan A, Chen X, Yang K et al. · Biomolecules · (2026) · View on PubMed ↗ · Free PDF ↗

Stroke drives glioma progression through the emergence of tumor-associated astrocytes with reduced Ca2+ activity.

This study investigated how stroke promotes glioma progression in human and mouse glioma models, focusing on the emergence of tumor-associated astrocytes (TAAs) with reduced Ca2+ activity at the invasive front. It found that stroke remodels the tumor microenvironment, increasing infiltration and survival disadvantage while inducing TAAs with diminished Ca2+ signaling and enriching tumor-associated microglia/macrophages (TAMs); restoring TAA Ca2+ signaling or depleting TAMs suppressed stroke-induced glioma progression. The scientific significance is that Ca2+-dependent TAA biology and TAMs become actionable mechanistic links between brain injury and glioma aggressiveness.

Ye Q, Madamba C, Woo J et al. · Nature cancer · (2026) · View on PubMed ↗

Recommendations for the management of frailty in chronic kidney disease: a consensus report.

This consensus report studied the management of frailty in chronic kidney disease (CKD), focusing on how to assess frailty, whether targeted interventions can reverse modifiable contributors, and how frailty should influence decisions between conservative kidney management and kidney replacement therapy (KRT). It found that frailty is common and prognostically important in CKD, but that evidence gaps remain regarding optimal assessment tools and intervention effectiveness, prompting 63 consensus statements across four domains. The clinical significance is that it provides a structured framework to standardize frailty evaluation and guide treatment planning in CKD care.

Li PK, Chan GC, McAdams-DeMarco M et al. · Nature reviews. Nephrology · (2026) · View on PubMed ↗ · Free PDF ↗

---

---

Generated automatically on September 28, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.