PubMed Trending Research Digest — July 06, 2026

Automated digest · 98 articles · 15 research areas · July 06, 2026

Overview

This week’s papers cluster around a shared push toward mechanism-informed, personalized medicine—whether in neurodegeneration, cancer, or cardiometabolic disease. In Parkinson’s disease, genetically defined iPSC models and post-mortem single-nucleus profiling converge on lysosomal/autophagy dysfunction and glial immune dysregulation as actionable biology, while population studies link sleep patterns to PD risk and provide more objective neurocognitive readouts.

In oncology, the dominant theme is exploiting vulnerabilities in regulated cell death and the tumor microenvironment. Multiple studies dissect how pathways such as PANoptosis, ferroptosis resistance (including MLKL–ESCRT-III membrane repair), and replication-stress control can be therapeutically targeted, while others show how macrophage or CAF programs (e.g., glutamine metabolism, GDF-15, PAI-1/EGFR signaling, and EV-mediated signaling) drive resistance, metastasis, and cachexia. Complementing these mechanistic advances, several clinical and translational efforts highlight evolving immunotherapy strategies—antibody-drug conjugate engineering, dendritic cell vaccination, and sequencing of T-cell–redirecting therapies—alongside safety-focused work (e.g., immune-mediated hepatotoxicity after AAV gene therapy).

Finally, cardiometabolic and immune research emphasizes practical risk stratification and modifiable pathways: composite inflammation/insulin-resistance indices for COPD and cardiovascular risk, life-course timing of MASLD for diabetes prediction, and incretin-based therapies (including pediatric and heart-failure contexts). Across microbiome and immune studies, gut microbial metabolites and barrier disruption repeatedly emerge as upstream drivers of autoimmune neuroinflammation and other inflammatory phenotypes, reinforcing the idea that diet-microbe-immune signaling is becoming a therapeutic target rather than just a correlation.

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Neurodegeneration & Tau Pathology

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

This study examined regional wasteosome (corpora amylacea) accumulation across neurodegenerative diseases to assess whether it reflects a shared mechanism potentially related to glymphatic insufficiency. The key finding was that wasteosome distribution patterns were compatible with chronic glymphatic clearance impairment across the investigated neurodegenerative contexts. Scientifically, it supports wasteosomes as a potential histopathological readout of glymphatic dysfunction and a unifying mechanism across multiple neurodegenerative diseases.

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.

In forebrain neurons of Tau4R; CaMKII-CreER; Tardbpf/f mice, the study tested whether TDP-43 loss-of-function (LOF) drives pathological conversion of tau and worsens neurodegeneration. TDP-43 LOF exacerbated tauopathy-dependent brain atrophy and was associated with increased vulnerability of specific neuron populations. These results strengthen the mechanistic link between TDP-43 dysfunction and tau pathology, suggesting that targeting TDP-43-related pathways could mitigate tau-driven neurodegeneration.

Baghel MS, Burns GD, Tsapatsis M et al. · Molecular neurodegeneration · (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 investigated early red/green (L/M) cone-competent precursor populations derived from human retinal organoids (ROs) and their axonogenesis/axon dynamics, aiming to identify donor cells for cone replacement. The authors report identification and enrichment of early L/M cone-competent precursors with intrinsically enhanced axon dynamics compared with later or less competent cone populations. This supports a cell-replacement strategy for foveal vision restoration by improving the likelihood of functional integration through superior axon outgrowth behavior.

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

An open dataset of cerebral tau deposition in young healthy adults based on [18F]MK6240 positron emission tomography.

The authors created an open dataset quantifying cerebral tau deposition in young healthy adults using [18F]MK6240 PET imaging. The dataset provides in vivo tau measurements with a second-generation tracer designed for high tau affinity and minimal off-target binding, enabling study of early tau pathophysiology before clinical neurodegeneration. This resource supports future mechanistic and biomarker research into tau accumulation in younger individuals and preclinical disease trajectories.

Lam J, Rodriguez-Cruces R, Arafat T et al. · Scientific data · (2026) · View on PubMed ↗ · Free PDF ↗

Joint trajectories of brain atrophy, white matter hyperintensities and cognition quantify brain maintenance.

This work developed a domain-general brain maintenance index by jointly modeling longitudinal brain atrophy (MTLV-ratio), white matter hyperintensities (WMH), and cognition (PACC5) using latent growth curve modeling in cognitively unimpaired older adults from the DELCODE cohort (n=543, 4-year follow-up). Changes in MTLV-ratio and WMH additively predicted cognitive outcomes, and the combined trajectories quantified brain maintenance more directly than single biomarkers. The approach provides a quantitative framework for tracking brain health and evaluating interventions aimed at preserving cognition during aging.

Menze I, Bernal J, Kievit RA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Neuroprotective potential of resveratrol in Parkinson, Huntington, amyotrophic lateral sclerosis, and multiple sclerosis: a comprehensive review.

This comprehensive review studied the neuroprotective potential of resveratrol across Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS), emphasizing mitochondrial and cellular stress pathways. It found that resveratrol enhances mitochondrial function via the AMPK/SIRT1/PGC-1α pathway, reduces α-synuclein accumulation (PD-relevant), and modulates autophagy, with improved effects reported for nano-resveratrol formulations and combination strategies (e.g., with L-DOPA or EGCG) in animal models. This is significant because it consolidates mechanistic evidence supporting resveratrol-based strategies as candidates for adjunct neuroprotection, while highlighting translational targets.

Shahsavari K, Yazarlu O, Ahmadnia H et al. · Molecular biology reports · (2026) · View on PubMed ↗

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Parkinson’s Disease Modeling, Biomarkers & Risk

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

The study used single-nuclear RNA sequencing on post-mortem Parkinson’s disease tissue to characterize altered microglial and astrocytic functions in the substantia nigra pars compacta (SNpc). It identified transcriptional changes consistent with dysregulated glial immune/inflammatory programs in PD compared with controls. These data provide molecular resolution of microglia–astrocyte dysfunction that may contribute to neurodegeneration and guide target discovery for PD therapies.

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

Sleep and Parkinson’s disease: a population-based study from the CHARLS cohort.

This population-based study used the China Health and Retirement Longitudinal Study (CHARLS, 2011–2020) to assess associations between sleep patterns and Parkinson’s disease (PD) risk in a Chinese community cohort. Sleep duration showed a significant age- and gender-dependent relationship with PD risk, with a negative association in participants aged ≤60 years and a U-shaped pattern in those >60 years. The results suggest that age- and sex-specific sleep targets may be important for PD prevention strategies in Chinese populations.

Wang Y, Lv W, Li Y et al. · NPJ Parkinson’s disease · (2026) · View on PubMed ↗ · Free PDF ↗

A PARK9 iPSC-Derived Dopaminergic Neuron Model Enables Drug Screening Targeting Autophagy-Lysosome Pathway Dysfunction in Parkinson’s Disease.

The study generated PARK9 patient-derived induced pluripotent stem cells (iPSCs) carrying an ATP13A2 mutation and mutation-corrected isogenic controls to model Parkinson’s disease dopaminergic neurons and test drugs targeting autophagy–lysosome pathway dysfunction. PARK9 iPSC-derived neurons showed lysosomal dysfunction with impaired lysosomal acidification and reduced mature cathepsin D levels, recapitulating disease-relevant phenotypes linked to autophagy–lysosome impairment. This iPSC model provides a human, genetically defined platform to screen and develop disease-modifying therapies aimed at lysosome/autophagy defects in Parkinson’s disease.

Tsukiboshi KI, Ishikawa KI, Yamaguchi A et al. · Journal of neurochemistry · (2026) · View on PubMed ↗

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Neuroinflammation & Infection-Driven Brain Injury

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, the study examined whether inhibiting the cGAS-STING pathway reduces neuroinflammation and cognitive impairment. The authors found increased cGAS and STING protein levels and elevated TBK1/IRF3 phosphorylation in the cerebral cortex, and pharmacological inhibition of cGAS-STING alleviated downstream neuroinflammatory effects and cognitive deficits. This supports cGAS-STING as a therapeutic target for infection-associated neuroinflammation and cognitive impairment.

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

Xuefu Zhuyu Decoction Ameliorates Neuroinflammation after Traumatic Brain Injury via tRF-3-Leu-AAG/Gpr17 axis.

Xuefu Zhuyu Decoction (XFZYD) was studied in traumatic brain injury (TBI) models to determine whether its anti-neuroinflammatory and neuroprotective effects involve epigenetic regulation via transfer RNA-derived small RNAs (tRFs/tsRNAs). XFZYD modulated the tRF-3-Leu-AAG/Gpr17 axis to reduce neuroinflammation and improve neurological recovery after TBI. This identifies a specific tsRNA–receptor pathway that could be leveraged to develop mechanism-based TBI therapeutics.

Yang Z, Yuan Z, Hou J et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

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Sleep & Oculomotor/Neurocognitive Biomarkers

Analysis of positional obstructive sleep apnea features in 12,000 patients at a sleep center.

This retrospective sleep-center study analyzed positional obstructive sleep apnea (POSA) features in 12,036 patients undergoing polysomnography to determine prevalence and clinical/polysomnographic characteristics. It found that 66.3% had POSA and 27.8% had supine-exclusive POSA, with POSA associated with lower AHI and BMI and with e-POSA being more frequent in women. This is clinically significant because it characterizes a large POSA phenotype distribution that can inform risk stratification and tailored management strategies.

Rosa CFA, Chillcce KAS, Cahali MB et al. · Sleep & breathing = Schlaf & Atmung · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluation of Oculomotor Function Following Sleep Improvement With Lemborexant in Older Adults With Insomnia.

In an open-label, single-arm study of 31 Japanese adults aged ≥50 years with insomnia, the researchers evaluated changes in oculomotor function after sleep improvement with lemborexant (5–10 mg nightly) at baseline, week 4, and week 12. Eye movements measured during free-viewing, smooth pursuit, and fixation tasks improved in parallel with sleep improvement following lemborexant treatment. These findings support oculomotor tasks as objective, treatment-sensitive biomarkers of neurocognitive state in older adults with insomnia.

Miyata S, Kawai K, Iwamoto K et al. · Human psychopharmacology · (2026) · View on PubMed ↗

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Gene Therapy Safety & Immune-Mediated Toxicity

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 used PBAE (poly(beta-amino ester)) nanoparticles to deliver ASCL1 and NGN2 genes for astroglia-to-neuron reprogramming after spinal cord injury, aiming to remodel glial scar. The key finding was that nanoparticle-mediated gene delivery enabled reprogramming toward a neuronal phenotype while addressing persistent barriers such as glial scar formation without relying on viral vectors. This is significant as a safer, non-viral gene delivery strategy to enhance functional neural repair after spinal cord injury.

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

Prolonged fenfluramine use in open-label studies of Dravet or Lennox-Gastaut syndromes: Long-term safety, tolerability, patient global functioning, and considerations for interpreting effectiveness.

In an international multicenter open-label extension (OLE; NCT03936777), this study reported long-term safety, tolerability, and patient global functioning in patients with Dravet syndrome (DS) or Lennox-Gastaut syndrome (LGS) treated with fenfluramine after prior open-label feeder studies. Fenfluramine was continued at the latest feeder dose and then flexibly titrated (with maximum dosing adjusted for concomitant stiripentol), and the study focused on sustained tolerability and global functioning over extended follow-up. The findings are important for clinicians interpreting long-term real-world effectiveness and safety of fenfluramine in these severe pediatric epilepsies.

Gil-Nagel A, Knupp KG, Gunning B et al. · Epilepsia · (2026) · View on PubMed ↗ · Free PDF ↗

Adeno-Associated Virus Gene Therapy for Spinal Muscular Atrophy Induces Hepatotoxicity via Cytokine and Macrophage Activation.

This report investigated immune mechanisms of hepatotoxicity in two spinal muscular atrophy patients who developed macrophage activation syndrome–like features shortly after AAV9 gene therapy with onasemnogene abeparvovec. The patients showed innate immune activation with marked hyperferritinemia and hepatotoxicity accompanied by thrombocytopenia, hypertriglyceridemia, and hypofibrinogenemia, with serial cytokine/chemokine surges and macrophage activation detected by flow cytometry. The results highlight cytokine- and macrophage-driven innate immune activation as a mechanistic basis for AAV9-associated liver toxicity, informing monitoring and risk mitigation strategies for gene therapy.

Sakai A, Sugiyama M, Onodera M et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗ · Free PDF ↗

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Immune Profiling & Sepsis Prognosis

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

In a multicentre prospective cohort of 1,851 adults aged ≥60 years (healthy controls, nonsevere infection, and sepsis), immune-inflammatory profiles were measured longitudinally to determine their relationship with in-hospital mortality. The study identified immune-cell subset, cytokine, complement, and routine laboratory patterns that distinguished sepsis from nonsevere infection and showed prognostic associations with subsequent mortality. These findings support immune-inflammatory profiling as a potential risk-stratification tool for older adults with sepsis.

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

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Regulated Cell Death (PANoptosis/Ferroptosis/Necroptosis) & Membrane Repair

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

This review studied protein lysine lactylation (Kla) across health and disease, focusing on the enzymes and molecular pathways that regulate lactylation writers, readers, erasers, and lactyl-CoA synthases. It found that Kla—driven by lactate-dependent enzymatic L-lactylation and potentially non-enzymatic routes—links cellular metabolism to epigenetic-like regulation and expands proteome function beyond histones to non-histone proteins. These mechanistic insights support Kla as a clinically relevant biomarker and therapeutic target across inflammatory, metabolic, and cancer contexts.

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

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

This work developed butyrylated PGAM5-triggered, glutathione (GSH)-responsive cysteine polymer nanoparticles (Cys8E@CBL0137) to deliver the antitumor agent CBL0137 for enhanced necroptosis in prostate cancer. The key finding was that exploiting high intracellular GSH enabled targeted intracellular delivery and increased tumor-killing efficacy, with the strategy designed around butyrylation-related and GSH-responsive mechanisms. Scientifically and clinically, it provides a nanoparticle delivery approach to overcome prostate cancer therapeutic resistance by promoting necroptosis through redox-responsive drug release.

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

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

Using human single-cell RNA-seq data from lung transplant ischemia-reperfusion injury (LTx-IRI) and a rat lung transplant model, the study tested whether the RIPK3 inhibitor GSK’872 mitigates IRI by modulating PANoptosis and inflammation in a cell type–specific manner. GSK’872 reduced injury when added to lung preservation solution and/or administered to recipients, with effects linked to suppression of PANoptosis- and inflammation-related gene programs across relevant parenchymal and inflammatory cell populations. This suggests GSK’872 as a mechanistically targeted therapeutic strategy to improve lung transplant outcomes by limiting regulated cell death and inflammatory cascades.

Li J, Ma X, Huang J et al. · Cell communication and signaling : CCS · (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 study investigated how MLKL (mixed lineage kinase domain-like protein) promotes ferroptosis resistance through impaired ESCRT-III–mediated membrane repair. The authors combined bioinformatics with mechanistic experiments to show that higher MLKL activity supports survival under ferroptosis-inducing stress by disrupting ESCRT-III-dependent membrane repair processes. This identifies an MLKL–ESCRT-III axis as a potential target to overcome ferroptosis resistance in colorectal cancer.

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

Unlocking the ferroptotic window: Lipidomic rewiring and metabolic addiction in EMT-driven breast cancer resistance.

The article (Perspective) analyzed how epithelial-mesenchymal transition (EMT), particularly partial EMT (p-EMT) states, creates a metabolic and iron-lipid vulnerability that opens a “ferroptotic window” in breast cancer resistance. It proposes a hierarchical logic in which progressive p53 alterations (from loss-of-function to gain-of-function) rewire lipid metabolism and iron regulation, converting p-EMT cells from passive sensitization to strong ferroptosis susceptibility. This frames ferroptosis as a targetable vulnerability in EMT-driven therapy resistance and highlights p53-driven metabolic rewiring as a key determinant of response.

Lu J, Filippopoulou C, Sun J et al. · Cell death discovery · (2026) · View on PubMed ↗ · Free PDF ↗

Dihydroberberine regulates the ferroptosis-autophagy positive feedback loop in colorectal cancer by targeting PANX2.

In colorectal cancer models, dihydroberberine was evaluated as a small-molecule modulator of the ferroptosis–autophagy positive feedback loop by targeting PANX2. The study reports that dihydroberberine regulates ferroptosis and autophagy through PANX2, disrupting the feedback circuitry that supports cancer cell survival. This positions PANX2 as a druggable target and dihydroberberine as a candidate ferroptosis-based therapeutic strategy for CRC.

Xu L, Meng Q, Wang F et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Nanozyme-Reinforced miR-197-3p Delivery Resets Metabolic and Senescence Pathways to Rejuvenate Osteoarthritic Cartilage.

Researchers developed a nanozyme-reinforced delivery system to deliver miR-197-3p to osteoarthritic cartilage and tested its effects on metabolic and senescence pathways. miR-197-3p was downregulated in aged and osteoarthritic cartilage, and its delivery rejuvenated cartilage by restoring extracellular matrix anabolism, suppressing senescence, and directly targeting G3BP1 to reduce redox imbalance and inflammatory signaling. This supports miR-197-3p as a cartilage-protective therapeutic target and the miR delivery platform as a potential disease-modifying approach for osteoarthritis.

Cai X, Lv Z, Zhang C et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Broussonin A Attenuates Type 2 Diabetic Osteoporosis by Reactivating JAK2/STAT3 Signaling to Inhibit Ferroptosis in BMSCs.

This study evaluated whether Broussonin A (BRA) attenuates type 2 diabetic osteoporosis (T2DOP) by reactivating JAK2/STAT3 signaling to inhibit ferroptosis in bone marrow mesenchymal stem cells (BMSCs). Using a rat T2DOP model induced by streptozotocin (STZ) plus a high-fat diet and an in vitro glucolipotoxicity-based BMSC model, BRA restored bone quality and suppressed ferroptosis through the JAK2/STAT3 pathway. The results are clinically relevant because they propose a mechanistic, pathway-targeted natural compound strategy to counter ferroptosis-driven bone deterioration in T2DOP.

Guo Y, Huang Y, Han L et al. · Phytotherapy research : PTR · (2026) · View on PubMed ↗

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Cancer Immunotherapy & Vaccine Strategies

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). The key finding was that the trial compared efficacy outcomes with a median follow-up of 21.4 months in 192 randomized patients, establishing the clinical performance of orelabrutinib against standard chemoimmunotherapy. Clinically, it informs first-line treatment selection for CLL/SLL by evaluating whether BTK-targeted therapy can improve outcomes relative to chlorambucil-rituximab.

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

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

This phase IIIb TOURMALINE study evaluated durvalumab combined with gemcitabine-based chemotherapy regimens in advanced biliary tract cancer (aBTC), including a close-to-real-world population with poor prognosis. The key finding from the primary results was the safety and efficacy profile of first-line durvalumab (1500 mg IV) plus investigator-selected gemcitabine-based regimens across seven chemotherapy options. Clinically, it extends evidence from TOPAZ-1 by testing durvalumab–chemotherapy in broader regimen choices and real-world-like patients.

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

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

As an AACR 2026 meeting update, the article reviewed advances in antibody-drug conjugates (ADCs) focusing on new design strategies and targeting approaches. Key themes included dual- and multi-payload ADCs, multispecific targeting, immunostimulatory payloads, and tumor microenvironment-directed strategies such as depletion of regulatory T cells and tumor-associated macrophages to address heterogeneity, resistance, and systemic toxicity. This highlights emerging ADC engineering directions likely to improve efficacy and safety in cancer therapy.

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

Adult acute lymphoblastic leukemia: incorporation of recent advances into current treatment strategies.

This article reviewed current treatment strategies for adult acute lymphoblastic leukemia (ALL), emphasizing how recent advances have changed outcomes. It highlights targeted therapies including BCR::ABL1 tyrosine kinase inhibitors for Philadelphia chromosome-positive ALL and immunotherapies such as CD19/20/22 antibodies and CAR T cells, as well as the bispecific T-cell engager blinatumomab improving survival in relevant patient groups. The review synthesizes how modern targeted and immune-based approaches are reshaping risk-adapted management of adult B-cell ALL.

Jabbour E, Kantarjian H · Blood cancer journal · (2026) · View on PubMed ↗ · Free PDF ↗

Cryo-EM structure of African horse sickness virus VP2 receptor-binding protein enables nanoparticle vaccine design.

The authors determined the 3.11 Å cryo-EM structure of full-length African horse sickness virus (AHSV) serotype 4 VP2, focusing on its receptor-binding protein architecture. Structure-guided mapping identified a VP2 subdomain targeted by neutralizing antibodies, enabling rational nanoparticle vaccine design against AHSV. This structural vaccinology work provides a concrete antigen blueprint for developing safer, non-attenuated vaccines for a lethal equine pathogen.

Martínez-Castillo A, Aebischer A, Toneatti P et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Personalized neoantigen-pulsed autologous dendritic cells in newly-diagnosed glioblastoma: a phase Ib trial.

The study evaluated safety and preliminary efficacy of personalized neoantigen-pulsed autologous dendritic cells (ZSNeo-DC) as an adjuvant therapy in newly diagnosed glioblastoma (nGBM) patients in a single-arm, open-label phase Ib trial. ZSNeo-DC was generally well tolerated with adverse events mostly grade 1–2 and only two grade 1–2 febrile events reported as treatment-related, with secondary analyses including progression-free survival. This supports the clinical feasibility of individualized neoantigen dendritic cell vaccination following surgery and standard radio-chemotherapy in nGBM and provides early safety signals for further development.

Zhang Y, Chi X, Liu K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Real-World Evidence of Immunotherapy Sequencing in Multiple Myeloma: Durable Responses With BCMA-Targeting Bispecific Antibodies Following Prior GPRC5D-Targeting Therapy.

The retrospective multicenter study evaluated safety and efficacy of BCMA-targeting bispecific antibodies (BsAbs) given after prior GPRC5D-targeting BsAbs in relapsed/refractory multiple myeloma (RRMM). In 26 patients, BCMA BsAbs produced durable responses after GPRC5D BsAbs, addressing an unmet need for optimized T-cell-redirecting therapy sequencing. This real-world evidence supports a potentially effective sequencing strategy for T-cell-redirecting therapies in RRMM and can guide future prospective studies on optimal order of antigen targeting.

Cazaubiel T, Touzeau C, Vincent L et al. · Clinical lymphoma, myeloma & leukemia · (2026) · View on PubMed ↗

Endogenous-metabolite-inspired polyamine-oleic acid lipids for safe mRNA delivery and PCSK9 gene editing.

Researchers developed endogenous-metabolite-inspired polyamine–oleic acid lipids (agmatine-, putrescine-, cadaverine-, spermidine-, and spermine–oleic acid) to form lipid nanoparticles for mRNA delivery and PCSK9 gene editing. Among candidates, agmatine–oleic acid (Agm-oa) produced LNPs with high mRNA encapsulation efficiency, uniform particle size, and strong in vitro transfection, enabling PCSK9 gene editing. This provides a potentially safer LNP platform for therapeutic mRNA delivery and genome editing targeting PCSK9.

Hou X, Gao X, Wang J et al. · Journal of controlled release : official journal of the Controlled Release Society · (2026) · View on PubMed ↗

Personalized therapy in metastatic hormone-sensitive prostate cancer: a 2026 update on navigating therapeutic complexity.

This review studied how biomarker-driven treatment selection is being integrated into combination strategies for metastatic hormone-sensitive prostate cancer (mHSPC) in the context of recent phase III trial data presented at ESMO 2025 and ASCO GU 2026. It found that therapeutic intensification is increasingly guided by tumor biology and biomarker-driven decision algorithms rather than clinical features alone, reflecting the growing complexity of doublet/triplet regimens. This matters clinically because it supports more personalized, biology-informed sequencing and combination choices to improve outcomes in mHSPC.

Koett M, Artamonova N, Heidegger I · Current opinion in urology · (2026) · View on PubMed ↗

Targeting SYK to alleviate MDSC-driven immunosuppression and augment anti-PD1 efficacy.

This preclinical study investigated whether targeting spleen tyrosine kinase (SYK) can reduce myeloid-derived suppressor cell (MDSC)-driven immunosuppression and thereby enhance anti–PD-1 therapy. Using a mouse model with a gain-of-function SYK^S544Y mutation and tumor models, it found that SYK activation promotes tumor progression largely through MDSC-dependent mechanisms and operates via the JAK–STAT–CXCR2 signaling axis. This is significant because it provides a mechanistic rationale for combining SYK inhibition with anti–PD-1 immune checkpoint blockade to improve antitumor immunity.

Zeng Z, Cao X, Li C et al. · Science China. Life sciences · (2026) · View on PubMed ↗

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Targeted Cancer Pathways & Resistance Mechanisms

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

This preclinical study investigated whether dihydroartemisinin (DHA) can inhibit mutant KRAS to overcome resistance to regorafenib plus anti-PD-1 in KRAS-mutant colorectal cancer liver metastases. The key finding was that DHA selectively downregulated KRASG12D (without affecting wild-type KRAS) and potentiated the antitumor activity of regorafenib plus anti-PD-1 in the liver metastasis setting. This is significant because it identifies a KRASG12D-targeted strategy using a clinically approved drug to improve immunotherapy–TKI combination efficacy in CRC liver metastases.

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

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

In T-cell acute lymphoblastic leukemia (T-ALL), the study tested whether therapeutic activation of PPARα suppresses NOTCH1 signaling using chiglitazar in Jurkat and Molt4 cell lines and in xenograft models (CDX and PDX). Using RNA-seq, qRT-PCR, Western blotting, luciferase reporter assays, DNA affinity precipitation, co-immunoprecipitation, and ChIP, the authors showed that chiglitazar inhibited NOTCH1 pathway activity and reduced leukemic cell viability/proliferation while promoting apoptosis in vitro and tumor control in vivo. This positions PPARα activation as a potential strategy to therapeutically downregulate NOTCH1-driven T-ALL.

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

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

The study examined how inhibiting poly(ADP-ribose) glycohydrolase (PARG) affects replication stress responses in cells, focusing on replication fork collapse and replication protein A (RPA) dynamics. PARG inhibition caused sustained PARylation that reduced phosphorylated and chromatin-bound RPA most strongly during fork-stalling-to-collapse, requiring PARP1 activity and being modulated by intact ATR–CHK1 checkpoint signaling. These findings support PARG inhibition as a replication-stress–targeting anticancer strategy by revealing a mechanistic vulnerability in fork collapse responses and RPA loading control.

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

The BRCA1-A complex restricts replication fork reversal-dependent DNA repair in ATM deficient cells.

This study investigated how the BRCA1-A complex influences replication fork reversal-dependent DNA repair in ATM-deficient cells. ATM inhibition triggered SUMO- and ubiquitin-mediated BRCA1-A damaged-fork recognition that restricted end resection and produced hypersensitivity to topoisomerase I inhibitors, with BRCA1-A deficiency showing increased chromatin accessibility and nuclease activity at damaged forks. The work clarifies a fork-repair control mechanism that could be exploited to improve therapeutic targeting of ATM-deficient tumors.

Datta A, Jackson J, Morozov YI et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

ZNF689 loss impairs homologous recombination sensitizing triple-negative breast cancer to combined PARP and PD-L1 inhibition.

The study examined the role of zinc-finger protein 689 (ZNF689) in homologous recombination (HR) and treatment response in triple-negative breast cancer (TNBC), including mechanistic experiments on DNA damage signaling. ZNF689 loss impaired HR by disrupting an ATM-dependent pathway in which ZNF689 is phosphorylated by ATM, promotes NBS1 ubiquitination via the E3 ligase SKP2, stabilizes the MRN complex, and supports ATM activation, thereby sensitizing TNBC to combined PARP and PD-L1 inhibition. These results identify ZNF689 as a potential biomarker and therapeutic vulnerability to enhance immunotherapy–PARP inhibitor synergy in BRCA-wild-type TNBC.

Ge LP, Xiao YL, Wu SY et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Activation of KIT signaling promotes early tumorigenesis through the AP-1 pathway in APC/TP53 double-knockout human colon organoids.

The study used CRISPR-Cas9 to generate APC/TP53 double-knockout human colon organoids and investigated how KIT signaling drives early tumorigenesis through the AP-1 pathway. Multi-omics profiling identified KIT as a key factor in the early-stage epigenetic and transcriptional program associated with APC/TP53 loss, linking receptor tyrosine kinase signaling to AP-1 activation. This provides a mechanistic model of early colorectal cancer initiation that could inform pathway-targeted prevention or early intervention strategies.

Choi Y, Kim E, Cho SY et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Piezo1 inhibition promoted MELK degradation and impeded influenza virus entry into host cells.

This study investigated the role of Piezo1 in respiratory epithelial cells during influenza infection and tested whether inhibiting Piezo1 can block viral entry in vivo. It showed that Piezo1 inhibition promoted MELK degradation and impeded influenza virus entry into host cells via the Piezo1–MELK axis, using gene-editing/proteomics approaches to define the mechanism. These results support Piezo1 as a host-targetable antiviral pathway for preventing influenza entry.

He J, Guo H, Lu K et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

CHPF2-driven chondroitin sulfation of Wnt1 promotes colorectal cancer progression and is targeted by ponicidin.

This study investigated how chondroitin polymerizing factor 2 (CHPF2)-driven chondroitin sulfation of Wnt1 promotes colorectal cancer progression and whether the compound ponicidin can target this pathway. CHPF2 was linked to worse prognosis, and ponicidin targeted CHPF2 to suppress chondroitin sulfate synthesis, thereby blocking the Wnt/β-catenin signaling pathway and reducing tumor-promoting behaviors. These results support CHPF2–Wnt1 chondroitin sulfation as a therapeutic vulnerability in colorectal cancer.

Ye Y, Liang Y, Lan H et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Relationships of serum cabozantinib concentration with tumor response and adverse events in treatment of advanced renal cell carcinoma: observational exploratory prospective study.

This prospective observational study examined relationships between serum cabozantinib trough concentrations and both tumor response and adverse events in 12 patients with advanced renal cell carcinoma treated with cabozantinib monotherapy. It found that cabozantinib exposure (trough levels) correlated with measures of tumor shrinkage and with the occurrence of adverse events, suggesting concentration-toxicity and concentration-response links. This is significant because it supports the potential for therapeutic drug monitoring to optimize cabozantinib dosing for efficacy while limiting toxicity.

Doke Y, Noda S, Kusaba T et al. · International journal of clinical oncology · (2026) · View on PubMed ↗ · Free PDF ↗

AI-based tumor and organ volumetry predicts early progression after Y-90 radioembolization in liver-dominant metastatic disease.

This retrospective study evaluated automated CT-based whole-liver tumor volumetry as a quantitative imaging biomarker in 57 adults with liver-dominant metastatic disease undergoing yttrium-90 (90Y) transarterial radioembolization (TARE). Automated volumetric changes in tumor, liver, and spleen were used to predict early progression after TARE, outperforming manual RECIST-based measurements in multifocal disease. These findings support AI-driven volumetry as a clinically actionable imaging tool for earlier risk stratification and response assessment in 90Y TARE patients.

Martinez Heinemann D, Bodden J, Endroes L et al. · European journal of nuclear medicine and molecular imaging · (2026) · View on PubMed ↗ · Free PDF ↗

Outcomes of maintenance BCG versus gemcitabine/docetaxel following BCG induction in NMIBC.

This study compared oncologic outcomes and safety of maintenance Bacillus Calmette-Guérin (BCG) versus gemcitabine/docetaxel (Gem/Doce) after BCG induction in treatment-naïve non-muscle-invasive bladder cancer (NMIBC), using data from 2016–2026. Maintenance Gem/Doce and maintenance BCG were evaluated for recurrence-free survival (RFS), high-grade RFS, progression-free survival, and metastasis-free survival, alongside systematically assessed adverse events. The findings aim to clarify whether Gem/Doce can match or improve efficacy and tolerability compared with continued BCG maintenance in NMIBC patients after induction BCG.

Gabriel PE, Zhu A, Karim CG et al. · BJU international · (2026) · View on PubMed ↗

Parathyroid Carcinoma: From Molecular Pathogenesis to Multidisciplinary Management.

This narrative review summarizes the molecular pathogenesis, diagnosis, imaging, and multidisciplinary management of parathyroid carcinoma (PC), emphasizing that CDC73 mutations with loss of parafibromin expression are central drivers. It also highlights emerging pathway alterations (PI3K/AKT/mTOR and Wnt) and discusses diagnostic suspicion criteria such as marked hypercalcemia, elevated PTH, palpable neck mass, and recurrent laryngeal nerve palsy, with localization using modalities including 99mTc-sestamibi, 4D-CT, and [18F]fluorocholine PET/CT. Clinically, the review consolidates actionable diagnostic and treatment strategies for a rare malignancy (<1% of primary hyperparathyroidism), supporting earlier recognition and appropriate surgical management (e.g., en bloc resection).

Song JX, Yang YY, Zhou JX et al. · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗

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Tumor Microenvironment (CAF/Macrophage/EVs/Stroma) & Metastasis

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

The study investigated how Foxs1 drives the transformation of CD34+ fibroblasts into myCAFs (Acta2+ cancer-associated fibroblasts) and how this promotes tumor growth, using inducible genetic lineage tracing, single-cell RNA sequencing, and spatial transcriptomics in melanoma and gastric cancer models. It identified Cd34+Pi16+ fibroblast progenitors and showed that upregulation of the transcription factor Foxs1 drives their differentiation toward Acta2+ CAFs. These findings define a developmental origin and transcriptional switch for pro-tumor CAF formation, highlighting Foxs1-mediated myCAF generation as a potential therapeutic target.

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

Signaling downstream of tumor-stroma interaction regulates mucinous colorectal adenocarcinoma apicobasal polarity.

The study analyzed patient-derived mucinous colorectal adenocarcinoma (MUC CRC) xenografts with apical-in versus apical-out polarity to determine how tumor–stroma signaling regulates epithelial polarity. Single-cell analyses identified α2β1-integrin as a collagen-binding receptor that activates Src and upregulates SorLA, promoting integrin recycling and HER signaling to support apical-in polarity. These findings link specific microenvironmental signaling (collagen–α2β1–Src–SorLA) to metastatic polarity programs, offering potential targets to influence prognosis in mucinous CRC.

Pasquier N, Pelkonen M, Carraz-Billat E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Reprogramming macrophage immunometabolism via glutamine antagonism potentiates colorectal cancer therapy in mice.

The study examined whether macrophage-targeted glutamine antagonism using a DON–artesunate conjugate (WGF-T17/T17) could reprogram tumor-associated macrophage immunometabolism and potentiate colorectal cancer therapy in mouse models. T17 blocked macrophage glutamine metabolism, shifting macrophages toward glycolysis with lactate accumulation and histone lactylation, which enhanced mitochondrial fission and phagocytic activity and improved anti-tumor therapeutic outcomes. This suggests a strategy to improve CRC immunotherapy by selectively targeting macrophage metabolic pathways (glutamine metabolism) to overcome a glutamine-high, immunosuppressive tumor microenvironment.

Fan R, Lu X, Zhang B et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

CAF-derived PAI-1 serves as an EGFR ligand and fuels KRAS-mutant pancreatic cancer.

The study investigated how cancer-associated fibroblast (CAF)-derived plasminogen activator inhibitor-1 (PAI-1) influences EGFR signaling and resistance to anti-EGFR therapy in KRAS-mutant pancreatic ductal adenocarcinoma (PDAC), using genetically engineered mouse models and patient-derived xenografts. CAF PAI-1 was selectively elevated in KRAS-mutant tumors and acted as an EGFR ligand, and stromal PAI-1 ablation disrupted CAF–tumor interactions and reduced tumor growth while enhancing the efficacy of anti-EGFR treatment. These findings identify a KRAS–c-Myc–linked stromal PAI-1/EGFR axis as a mechanism of anti-EGFR resistance and a potential therapeutic target in KRAS-mutant PDAC.

Wang Y, Liu C, Gao S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

CSF1R regulates monocyte subset differentiation and intracellular metabolism.

The study examined how CSF1R (CD115) controls monocyte subset differentiation and intracellular metabolism in mice, using acute CSF1R blockade and genetic deletion. CSF1R inhibition reduced blood Ly6Clow patrolling monocytes and impaired monocyte intracellular metabolism, in part by blunting differentiation-related processes (as described in the truncated mechanistic results). These findings establish CSF1R as a regulator linking monocyte maturation programs to metabolic state, with implications for targeting CSF1R in inflammatory and vascular contexts.

Gallerand A, Merlin J, Caillot Z et al. · Nature communications · (2026) · View on PubMed ↗

Targeting lipoprotein lipase-positive macrophage-driven GDF-15 expression alleviates cancer Cachexia in obese head and neck squamous cell carcinoma.

This study examined how targeting lipoprotein lipase-positive (LPL-positive) macrophage-driven GDF-15 expression affects cancer cachexia in obese head and neck squamous cell carcinoma (HNSCC). It identified an LPL-positive macrophage population enriched in tumors from overweight/obese settings and showed that suppressing this macrophage-GDF-15 axis alleviated cachexia phenotypes in obese HNSCC models. The work suggests a macrophage-targeted GDF-15 intervention strategy to improve outcomes in cachexia-prone obese HNSCC patients.

Guo YJ, Zhao R, Li YH et al. · Cellular signalling · (2026) · View on PubMed ↗

Small Extracellular Vesicle-TLN1 Modulates Gastric Cancer Cells and Remodels Lymphatic Endothelial Cells Through AKT Activation to Potentiate Lymphatic Metastasis.

This mechanistic cancer biology study investigated how small extracellular vesicles (sEVs) carrying TLN1 influence gastric cancer metastasis in vitro and in patient-relevant contexts. TLN1 was selectively enriched in sEVs from highly lymph-metastatic gastric cancer cells and in serum from gastric cancer patients with lymph node metastasis, and sEV-mediated TLN1 signaling promoted gastric cancer cell proliferation/migration/invasion/adhesion while remodeling lymphatic endothelial cells via AKT activation to potentiate lymphatic metastasis. The work identifies an sEV–TLN1–AKT axis as a potential therapeutic target to limit lymphatic spread in gastric cancer.

Li Y, Wen J, Cao X et al. · Cell biology international · (2026) · View on PubMed ↗

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Cardiometabolic Risk, Inflammation Indices & Fatty Liver

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

The study tested whether combined SGLT2 inhibitor and GLP-1 receptor agonist (SGLT2i + GLP-1Ra) therapy synergistically suppresses monocyte activation and prevents endothelial dysfunction in coronary artery disease (CAD), including both systemic inflammation–mediated and monocyte-driven mechanisms. In analyses across healthy individuals and patients with cardiovascular disease with and without CAD, the combined targeting reduced inflammatory activation of circulating monocytes and attenuated endothelial dysfunction more effectively than single-pathway approaches. This provides mechanistic support for dual SGLT2/GLP-1 targeting as a strategy to reduce residual inflammation–driven vascular injury in CAD.

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

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

This multi-center cohort study compared insulin resistance–related cardiovascular risk indices—triglyceride-glucose (TyG)-related indices, atherogenic index of plasma (AIP), and cardiometabolic index (CMI)—for predicting adverse cardiovascular events in people with NAFLD versus MASLD. The authors assessed whether the prognostic associations of these indices remain consistent when applying the newer MASLD framework rather than the older NAFLD definition. The findings help clinicians choose and interpret practical surrogate markers of cardiometabolic risk across evolving fatty-liver disease diagnostic criteria.

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

Beyond therapeutic maximalism: Prioritization and personalization in preventive therapies.

This article reviewed the shift from “therapeutic maximalism” to prioritization and personalization in preventive therapies, using modern lipid management as the main example. It emphasized that multi-axis lipid targeting (LDL-C, triglyceride-rich lipoproteins, lipoprotein(a), and vascular inflammation) enabled by agents such as PCSK9-targeted siRNA, CETP inhibitors, and Lp(a)-directed antisense/RNA therapies increases complexity and adherence challenges. The clinical significance is a call to tailor preventive regimens to patient risk, treatment burden, and feasibility rather than escalating therapy uniformly.

Sethi Y, Mahajan K, Shapiro MD et al. · Progress in cardiovascular diseases · (2026) · View on PubMed ↗

Association of metabolic dysfunction-associated steatotic liver disease onset age with risk of incident type 2 diabetes.

This prospective Kailuan Study analyzed whether the onset age of metabolic dysfunction-associated steatotic liver disease (MASLD) predicts incident type 2 diabetes (T2D) in 58,814 MASLD- and T2D-free participants. MASLD onset age was associated with the risk of developing incident T2D during follow-up, with earlier/later onset modifying diabetes risk (after excluding T2D cases occurring within the first 2 years). These findings suggest that MASLD timing across the life course can refine T2D risk stratification and prevention strategies.

Huo Z, Li Y, Liu T et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

Non-invasive imaging of atherosclerosis progression and cardiovascular outcome: a systematic review and meta-analysis.

This systematic review and meta-analysis studied whether non-invasive imaging measures of atherosclerosis progression are associated with subsequent cardiovascular outcomes as potential surrogate endpoints in clinical trials. Across 34 observational studies (n=56,189), it found modality-specific associations between imaging-defined progression and adverse cardiovascular events after multivariable adjustment. This is important for cardiovascular research because it evaluates the evidence base for using imaging progression as a surrogate endpoint rather than waiting for hard clinical outcomes.

El Youssef YW, Kühl JT, Abdulla J et al. · The international journal of cardiovascular imaging · (2026) · View on PubMed ↗

Association of C-Reactive Protein-Triglyceride Glucose Index With Chronic Obstructive Pulmonary Disease: Results From the NHANES and CHARLS Cohorts.

This study assessed whether the C-reactive protein–triglyceride glucose index (CTI) is associated with chronic obstructive pulmonary disease (COPD) prevalence in 8682 participants from CHARLS (China) and 8986 from NHANES (US) using multivariable logistic regression. Higher CTI was associated with greater odds of COPD, supporting CTI as a composite biomarker reflecting inflammation and insulin resistance relevant to COPD risk. Clinically, CTI could help stratify COPD risk using routine blood-based measures, potentially improving identification of individuals with inflammation/insulin-resistance–driven disease biology.

Gan J, Chen L, Zhu Y · Mediators of inflammation · (2026) · View on PubMed ↗ · Free PDF ↗

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Diabetes/Obesity Therapies (GLP-1, SGLT2, Incretins) & Metabolic Effects

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

This study tested whether liquiritigenin (LQ), a licorice-derived flavonoid, ameliorates high-fat-diet (HFD)-induced adipocyte insulin resistance in obese mice and in vitro co-culture systems. The key finding was that LQ improved glucose tolerance and insulin sensitivity while reducing inflammatory macrophage polarization by regulating the mtROS/OXPHOS axis. This is significant because it links a specific mitochondrial ROS/oxidative phosphorylation pathway to macrophage-driven insulin resistance and supports LQ as a candidate metabolic anti-inflammatory therapy.

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

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 experimental studies manipulating eccentric phase tempo in resistance training to assess acute neuromechanical responses and short-term recovery (immediately post-exercise to 7 days) in healthy adults who were trained or recreationally active. Across included protocols, the review evaluated how eccentric phase duration affects neuromuscular fatigue and indirect markers of exercise-induced muscle damage and recovery outcomes. The synthesis informs evidence-based programming of eccentric tempo to optimize training stimulus and short-term recovery.

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

GLP-1 receptor agonists in pediatric obesity.

This review summarized evidence on GLP-1 receptor agonists for pediatric obesity, focusing on efficacy, safety, and emerging combination strategies. It highlighted that liraglutide and semaglutide have demonstrated clinically meaningful weight-related benefits in adolescents and have regulatory approvals for patients ≥12 years, while common safety concerns primarily involve gastrointestinal adverse events. The review frames GLP-1RA therapy as an expanding pediatric obesity option with ongoing trials exploring combinations with other agents or bariatric surgery.

Abodi M, Agostoni CV, Mazzocchi A · Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonist Therapy in Children and Adolescents with Obesity: A Network Meta-Analysis of Differential Cardiometabolic Efficacy and Safety Profiles.

This network meta-analysis compared randomized trials of GLP-1 receptor agonists in adolescents with overweight or obesity, with and without type 2 diabetes, to assess differential cardiometabolic efficacy and safety across agents. The study found that specific GLP-1RAs differed in their cardiometabolic effects and tolerability profiles, supporting agent-level personalization rather than a single “class-wide” expectation. These comparative results can guide clinicians in selecting the most appropriate GLP-1RA for pediatric cardiometabolic risk reduction while balancing safety considerations.

Li Y, Xu X, Tuersun A et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Time to benefit of incretin-based therapies in adiposity-related heart failure with mildly reduced or preserved ejection fraction: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated the time to clinical benefit of incretin-based therapies—semaglutide and tirzepatide—in adults with overweight/obesity and heart failure with mildly reduced or preserved ejection fraction (HFmrEF/HFpEF, EF>40%) using randomized controlled trials with ≥52-week follow-up. The analysis estimated when incretin therapy begins to reduce worsening heart failure events compared with control. Clinically, defining “time to benefit” can guide expectations and treatment timing for semaglutide/tirzepatide in obesity-related HFmrEF/HFpEF.

Spiazzi BF, Zingano CP, Vest AR · Journal of cardiac failure · (2026) · View on PubMed ↗

A cold-induced GDF15-secreting adipocyte subpopulation regulates energy homeostasis through endocrine signaling.

This study examined how cold exposure reshapes brown adipose tissue (BAT) cell states in Ucp1 knockout mice using single-nucleus RNA sequencing to identify a distinct brown adipocyte subpopulation (U2). It found that U2 adipocytes secrete batokines enriched for growth differentiation factor 15 (GDF15) and that endocrine signaling via the GDF15–GFRAL axis regulates energy homeostasis. This is significant because it reveals a UCP1-independent thermometabolic control pathway that could be targeted to treat metabolic disease.

Wu C, Wang T, Gong S et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Exercise remodels the skeletal muscle immune microenvironment to ameliorate type 2 diabetes mellitus-induced muscle atrophy: From immunometabolism to organ crosstalk.

This review studied immunometabolic mechanisms linking type 2 diabetes mellitus (T2DM) to skeletal muscle immune microenvironment remodeling and diabetic sarcopenia, focusing on immune cell–myocyte crosstalk and how exercise alters these pathways. It found that T2DM-associated muscle atrophy involves coordinated immune dysregulation—including macrophage M1/M2 imbalance, mast cell/histamine signaling, NLRP3 inflammasome-driven pyroptosis, T-cell immunosenescence, and chemokine-driven inflammation—while exercise can ameliorate these changes. This matters scientifically and clinically because it frames exercise as a mechanistic intervention to restore immune-metabolic balance and reduce muscle wasting in T2DM.

Pengyu F, Huiyun X, Lijing G · Reviews in endocrine & metabolic disorders · (2026) · View on PubMed ↗

GLP-1 receptor agonists at immune checkpoint inhibitor initiation with immune-related and supportive-care outcomes in patients with cancer and overweight or obesity without diabetes: a target trial emulation.

This target trial emulation study examined whether GLP-1 receptor agonist (GLP-1 RA) use at immune checkpoint inhibitor (ICI) initiation is associated with wasting-related outcomes in adults with cancer and overweight/obesity without diabetes. Using TriNetX US data and excluding baseline diabetes with a 90-day GLP-1 RA wash, it assessed links between GLP-1 RA exposure at ICI start and wasting-related diagnoses and acute-care utilization. This is significant because it tests a potentially modifiable metabolic intervention that could influence sarcopenia/cachexia risk during ICI therapy.

Lin YJ, Li PY, Chen SC et al. · Cancer immunology, immunotherapy : CII · (2026) · View on PubMed ↗ · Free PDF ↗

Repurposing Metformin to Promote Fracture Callus Maturation via AMPK-Driven Metabolic Activation.

This preclinical study tested whether repurposed metformin accelerates fracture repair by promoting fracture callus maturation through AMPK-driven metabolic activation in a rat open femoral shaft fracture model. Compared with vehicle-treated controls, systemic metformin markedly accelerated callus maturation at 6 weeks, supported by histology, immunofluorescence, micro-CT, and biomechanical testing. These findings are significant because they suggest a clinically available drug could be leveraged to enhance bone healing by targeting metabolic bottlenecks in the repair process.

Pastukh V, Zhang J, Alexander PG et al. · Journal of orthopaedic research : official publication of the Orthopaedic Research Society · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular Devices & Pacing

Real-time algorithm-driven ventilation feedback to improve lung-protective ventilation in patients with ARDS (REALVENT-study): study protocol for a multicentre randomised controlled trial.

This multicentre randomized controlled trial protocol (REALVENT-study) studied whether a real-time, cloud-based algorithmic ventilation feedback platform can improve delivery of lung-protective ventilation in mechanically ventilated ARDS patients. The key finding is the trial design intent: to test whether actionable real-time feedback increases adherence to low tidal volume and driving pressure targets and improves clinical outcomes. Clinically, it targets a practical implementation gap by enabling continuous monitoring and decision support at the bedside.

Su L, Yang Y, Wang Y et al. · Respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗

Conduction system pacing versus biventricular pacing for cardiac resynchronization therapy: frequentist and bayesian meta-analysis of randomized controlled trial and propensity matched studies.

This meta-analysis compared conduction system pacing (CSP)—including left bundle branch pacing (LBBP), His bundle pacing (HBP), and HOT/LOT CRT—with biventricular (BiV) pacing for cardiac resynchronization therapy using both frequentist and Bayesian methods across randomized controlled trials and propensity-matched studies. CSP was associated with improved CRT response and clinical response compared with BiV pacing. These findings support CSP as a potentially more effective pacing strategy for CRT candidates, informing device-selection decisions.

Pranata R, Huang W, Tristan CD et al. · Heart rhythm · (2026) · View on PubMed ↗

Microsurgical Anatomy and Surgical Relevance of the Internal Frontal Arteries: A Cadaveric Anatomic Study.

This cadaveric anatomic study examined the microsurgical anatomy and morphometric variability of the anterior (AIFA), middle (MIFA), and posterior (PIFA) internal frontal arteries in 17 formalin-fixed, latex-injected cadaveric heads (29 hemispheres). The AIFA, MIFA, and PIFA were identified in 96.5%, 93.1%, and 96.5% of hemispheres, with common origins for AIFA and MIFA from the callosomarginal artery and PIFA frequently arising from the A4 segment. These detailed vascular maps and variability data are clinically significant for planning safer neurosurgical approaches involving internal frontal arterial branches.

Georgountzos G, Alexiadis I, Triantafyllou G et al. · The Journal of craniofacial surgery · (2026) · View on PubMed ↗

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Autoimmunity & Immune-Mediated Disease Mechanisms

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

RankVar, a random-forest machine learning model, was developed to prioritize causative variants for rare genetic diseases using clinical notes plus whole-genome/exome sequencing profiles in datasets spanning ~260 pediatric subjects for testing. The model was trained on ~1 million variants from the 1000 Genomes Project with spiked-in pathogenic variants and improved variant ranking by integrating external phenotype/clinical knowledge with variant features. This provides a scalable approach to reinterpret sequencing variants for rare-disease diagnosis and gene discovery by better leveraging phenotype-informed prior knowledge.

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.

This literature-based data analysis synthesized genetic abnormalities reported in patients with autism spectrum disorder (ASD) across studies published from 2020 onward. The review summarized the genetic architecture of ASD by cataloging recurrent categories of genetic variation and their reported associations with ASD risk factors. The work helps consolidate current evidence on ASD genetics to guide future mechanistic studies and variant interpretation frameworks.

Ręka G, Wojciechowska K, Lejman M · BMC medical genomics · (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 examined a murine model of eosinophilic chronic rhinosinusitis (ECRS) induced by topical calcipotriol and ovalbumin followed by intranasal ovalbumin challenges, assessing changes in the olfactory bulb (OB) and olfactory epithelium (OE). It found dysregulated glial and periglomerular cell states in the OB alongside altered lipocalin expression in the OE that together underlie olfactory dysfunction. These findings implicate specific central (glial/periglomerular) and peripheral (lipocalin) pathways as mechanistic targets for treating type 2 inflammation–associated 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.

This real-world retrospective study evaluated the effect of the GLP-1 receptor agonist semaglutide on blood eosinophil levels in adults and sought clinical/metabolic determinants of eosinophil reduction. Semaglutide treatment was associated with decreased eosinophil levels, with baseline clinical and metabolic factors linked to the magnitude of eosinophil change. The results suggest a potential anti-eosinophilic immunomodulatory effect of GLP-1RAs that could be relevant for eosinophilic airway disease phenotypes.

Wu Y, Lin Y, Wu J et al. · BMC pulmonary medicine · (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/clinical and genetic data to determine whether VEO-ADPKD shows a distinct genotype and more severe renal trajectory. Clinically, the results support risk stratification for early-onset ADPKD and inform prognosis and counseling for affected children and families.

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

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

This article presents an AI-augmented review that integrates childhood atopic dermatitis (AD) biomarker evidence across genetic, immune, microbial, and metabolic domains. The key output is a systems-level synthesis that compares biomarkers across domains while distinguishing evidence strength and improving scalability beyond manual review. Scientifically, it helps prioritize the most credible biomarker candidates and clarifies how multi-domain mechanisms may converge in pediatric AD.

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

Targeted long-read sequencing enables comprehensive analysis of the genetic and epigenetic landscape of inherited myopathies.

The study developed and validated a targeted long-read sequencing assay and bioinformatics framework to comprehensively characterize genetic variants and epigenetic signatures underlying inherited myopathies. The approach was designed to capture difficult variant classes (including repeat expansions and complex events such as D4Z4 contraction and associated hypomethylation) that are challenging for short-read next-generation sequencing. This provides a more complete molecular diagnostic tool for inherited myopathies by integrating sequence and epigenetic detection in a single targeted long-read workflow.

Yeow D, Reis ALM, Stevanovski I et al. · Nature communications · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

The BZR1-BLH1-PIF4 feedback module acts as a molecular amplifier for precise thermomorphogenesis in Arabidopsis.

The study investigated the molecular mechanism controlling Arabidopsis thermomorphogenesis by identifying the BEL1-LIKE HOMEODOMAIN transcription factor BLH1 as part of a BZR1–BLH1–PIF4 regulatory feedback module. BLH1 acted as a negative regulator of thermomorphogenesis, where BLH1 overexpression conferred high-temperature insensitivity and higher-order blh mutants showed high-temperature hypersensitivity, with BLH1 expression directly regulating the module. This clarifies how transcription factor feedback (BZR1–PIF4 via BLH1) enables precise temperature-responsive growth, informing strategies for climate-resilient crop engineering.

Qin W, Yin Q, Wang N et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Effectiveness and safety of mirikizumab in multirefractory ulcerative colitis: analysis from a real-world cohort.

The study assessed real-world effectiveness and safety of mirikizumab, an anti-IL-23 monoclonal antibody, in multirefractory ulcerative colitis (UC) patients. Using an observational cohort design, it evaluated clinical activity with partial Mayo (pMayo) scores at baseline, Week 12, and Week 24, along with urgency, biomarkers, endoscopic activity, and safety outcomes, including steroid-free clinical remission and response definitions. This provides practical evidence on how mirikizumab performs outside registration trials in a difficult-to-treat population and informs real-world expectations for efficacy and tolerability.

Melotti L, Monicelli O, Dussias NK et al. · Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · (2026) · View on PubMed ↗ · Free PDF ↗

Sinomenine regulates the AKT/FOXO3/GLUL pathway to inhibit pulmonary fibroblast-to-myofibroblast transition via α7nAChR against rheumatoid arthritis associated interstitial lung disease.

This mechanistic study investigated sinomenine (SIN) in rheumatoid arthritis-associated interstitial lung disease (RA-ILD), focusing on pulmonary fibroblast-to-myofibroblast transition and the α7 nicotinic acetylcholine receptor (α7nAChR) pathway. SIN inhibited the fibroblast-to-myofibroblast transition by regulating the AKT/FOXO3/GLUL axis downstream of CHRNA7 (α7nAChR), identifying GLUL as a crucial mediator linking RA and ILD. Targeting the α7nAChR–AKT/FOXO3–GLUL signaling network with SIN may represent a therapeutic strategy to treat RA-ILD fibrosis.

Liu M, Du H, Zheng J et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

RNA Sequencing Indicates Distinct Platelet Transcriptomic Changes in Immune Thrombocytopenia.

This study used RNA sequencing to characterize platelet-intrinsic transcriptomic changes in immune thrombocytopenia (ITP) and to determine whether these changes are distinct from non-immune thrombocytopenia. Platelets from patients with active ITP showed disease-associated transcriptomic alterations compared with chemotherapy-induced thrombocytopenia controls, indicating platelet RNA signatures that may contribute to ITP pathogenesis. The findings provide a molecular basis for distinguishing immune-specific platelet biology and for developing transcriptome-informed biomarkers or mechanisms in ITP.

Georgi JA, Hartwig M, Friedrich UA et al. · Journal of thrombosis and haemostasis : JTH · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of nutritional interventions on biomarkers of cellular senescence in humans: a systematic review.

This systematic review evaluated human interventional studies to determine whether nutritional interventions alter biomarkers of cellular senescence. Across included trials, it synthesized evidence on senescence-associated biomarkers measured in humans, assessing which nutritional strategies show potential senescence-modulating effects. The clinical significance is that it clarifies the current strength of evidence for nutrition as an intervention to influence human aging biology via cellular senescence markers.

Lin Y, Altulea A, Demaria M · Ageing research reviews · (2026) · View on PubMed ↗ · Free PDF ↗

Randomized trial comparing 5-year follow-up of first-line infliximab to conventional therapy in paediatric Crohn’s disease.

In the multicentre, open-label TISKids randomized trial, newly diagnosed, untreated pediatric Crohn’s disease patients aged 3–17 years (wPCDAI>40) were assigned to first-line infliximab (FL-IFX; five infusions then stopped) versus conventional therapy (exclusive enteral nutrition or prednisolone), with both arms receiving azathioprine maintenance. The study reports 5-year outcomes comparing sustained clinical remission without treatment escalation between strategies. If confirmed, these long-term data support optimizing early biologic use (infliximab) to improve durable disease control in children with moderate-to-severe Crohn’s disease.

Vuijk SA, Jongsma MME, Cozijnsen MA et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗ · Free PDF ↗

FCGR2A promoter variant reveals shared genetic susceptibility between IBD and stroke.

This genetic study investigated shared susceptibility between inflammatory bowel disease (IBD) and stroke by analyzing genome-wide association study (GWAS) summary statistics and applying Mendelian randomization (MR) plus colocalization to identify causal variants. It found that a FCGR2A promoter variant contributes to cross-trait genetic overlap between IBD and stroke, supported by functional prediction and in vitro experimental verification. This is clinically significant because it implicates FCGR2A regulatory biology as a mechanistic bridge between inflammatory disease and cerebrovascular risk.

Wang X, Zhu Z, Li H et al. · Molecular and cellular biochemistry · (2026) · View on PubMed ↗

Profiling the long-term risk of severe adverse events in a cohort of multiple sclerosis patients treated with different treatment sequences: Results from the Italian Multiple Sclerosis and Related Disorders Registry (I-MS&RD) (ProSA study).

Using the Italian Multiple Sclerosis and Related Disorders Registry (I-MS&RD; ProSA study), this analysis compared long-term incidence of infections and neoplasms across six disease-modifying therapy (DMT) sequences in real-world multiple sclerosis patients treated with moderate-efficacy treatment (MET), continuous high-efficacy therapy (C-HET), or pulsed high-efficacy therapy (P-HET). The study reconstructed treatment sequences (MET-only, C-HET-only, P-HET-only, MET→C-HET, MET→P-HET, and P-HET→MET) and estimated infection/neoplasm incidence rates per 1000 person-years for each sequence. The results provide evidence to better balance early intensive treatment strategies with long-term safety considerations when choosing between escalation and early high-efficacy approaches.

Paolicelli D, Lucisano G, Manni A et al. · Multiple sclerosis (Houndmills, Basingstoke, England) · (2026) · View on PubMed ↗

Reduced penetrance in genetic ALS/FTD spectrum disorders: implications for genetic counseling, predictive testing and treatment.

This review synthesized evidence on genetic ALS/FTD spectrum disorders showing that pathogenic variants often have reduced penetrance, including the C9orf72 repeat expansion, despite wide variation in earlier penetrance estimates. The key conclusion is that most pathogenic variants detected in clinical testing exhibit reduced penetrance, which complicates counseling and predictive testing. Clinically, this supports more transparent, probabilistic risk communication and careful interpretation of genetic test results for ALS/FTD patients and families.

Harrington EA, Dratch L, Jones TA et al. · Amyotrophic lateral sclerosis & frontotemporal degeneration · (2026) · View on PubMed ↗

A causal association between Epstein-Barr virus infection and lung cancer: A two-sample Mendelian Randomization study.

This two-sample Mendelian randomization (MR) study tested whether Epstein-Barr virus (EBV) infection has a causal effect on lung cancer risk using GWAS summary statistics for EBV exposure and lung cancer outcomes from the Finnish database. Using inverse-variance weighted (IVW) as the primary method with sensitivity analyses (weighted median, MR-Egger, and weighted mode) to assess robustness and pleiotropy, the study found a causal association between EBV infection and lung cancer. These results strengthen the causal inference beyond observational correlations and may inform future EBV-targeted prevention or risk stratification strategies for lung cancer.

Wang J, Wang K, Wang Z · Cancer biomarkers : section A of Disease markers · (2026) · View on PubMed ↗ · Free PDF ↗

The Tunneled Coronally Advanced Flap (TCAF) for Root Coverage Procedures: Rationale, Indications, and a Novel Papilla-Based Decision Tree.

This technical report described the clinical rationale and indications for the Tunneled Coronally Advanced Flap (TCAF) in root coverage procedures and proposed a novel papilla-based decision tree to guide selection between open versus tunnel approaches. The key contribution is the decision framework that tailors the surgical strategy to individual papilla characteristics. This is clinically significant because it standardizes decision-making and may improve predictability of periodontal root coverage outcomes.

Tavelli L, Barootchi S · Journal of periodontal research · (2026) · View on PubMed ↗ · Free PDF ↗

The Extra X Chromosome and Autoimmune Susceptibility in Klinefelter Syndrome.

This systematic review and meta-analysis quantitatively evaluated the association between Klinefelter syndrome (47,XXY) and autoimmune susceptibility by searching PubMed/MEDLINE, Scopus, and Web of Science through April 30, 2026 and pooling odds ratios using random-effects models. The analysis synthesized evidence across autoimmune diseases and autoimmune serological markers in individuals with Klinefelter syndrome, with prespecified subgroup analyses by outcome definition. The results provide an evidence-based estimate of autoimmune risk in Klinefelter syndrome, supporting more informed screening and clinical management of autoimmune comorbidities.

Gatta E, Delbarba A, Maltese V et al. · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Pathophysiology-Based Classification of Male Infertility: Evidence from an 800-patient Prospective Cohort.

This prospective monocentric cohort study enrolled 800 male partners of infertile couples and used comprehensive evaluation beyond semen analysis to develop a pathophysiology-based classification of male infertility. By phenotyping endocrine and mechanistic contributors, the study aimed to reduce the proportion of cases labeled idiopathic and to enable more targeted management aligned with underlying pathophysiology. Scientifically, it provides a framework for moving from semen-based labeling to mechanism-based stratification in male infertility.

Grande G, Graziani A, Caretta N et al. · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Microbiome-Gut-Immune-Endocrine Axis

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

This NHANES-based real-world study examined associations between probiotic, prebiotic, and yogurt (fermented food) consumption and colorectal cancer (CRC) prevalence in U.S. adults aged ≥50 years using dietary intake data from 2001–2020. The key finding was the reported relationship between these dietary exposures and CRC prevalence in the analyzed population (with results derived from observational NHANES data). Scientifically and clinically, it supports further investigation of gut-microbiota-modulating diets as potential CRC risk modifiers and helps generate hypotheses for future prospective studies.

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

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

The study evaluated anti–Helicobacter pylori activity of a molecularly identified Limosilactobacillus fermentum isolate and tested synergistic efficacy when combined with multiple antibiotics against clinical H. pylori isolates. It found that the L. fermentum isolate enhanced or synergized with antibiotic regimens to improve anti-H. pylori effectiveness in vitro. This supports development of adjunct probiotic-based combination therapies to help overcome antibiotic resistance in H. pylori infection.

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

The Microbiome-Gut-Gonad Axis: How Microbial Metabolites Orchestrate Reproductive Physiology, Pathology, and Therapy.

This review synthesized evidence for the Microbiome-Gut-Gonad axis, describing how gut microbial metabolites influence reproductive physiology and pathology and how these pathways may be targeted therapeutically. It highlighted mechanistic roles for specific metabolite classes (e.g., short-chain fatty acids) in regulating reproductive endocrine function and disease processes beyond simple correlation. The framework supports metabolite- and microbiome-directed interventions as potential approaches for endocrine and reproductive disorders.

El-Sehrawy AAMA, Oriquat G, Rizaev J et al. · The Journal of steroid biochemistry and molecular biology · (2026) · View on PubMed ↗

Mucin degradation by Akkermansia muciniphila promotes Alistipes-dependent tryptophan metabolism and Th17-driven autoimmunity.

This study examined how Akkermansia muciniphila-mediated mucin degradation influences Alistipes-dependent tryptophan metabolism and Th17-driven autoimmunity in a multiple sclerosis context. In relapsing-remitting MS patients and in the experimental autoimmune encephalomyelitis (EAE) model, A. muciniphila colonization worsened disease and was associated with enhanced Th17 responses, linking gut barrier disruption to pro-inflammatory immune activation. The results implicate A. muciniphila–tryptophan–Th17 pathways as potential therapeutic targets to modulate autoimmune neuroinflammation.

Lin X, Singh A, Shan X et al. · Mucosal immunology · (2026) · View on PubMed ↗

Panax quinquefolius saponins promote remyelination via orchestrating HMGCS1-NPC1-MAL-mediated lipid metabolism and rebalancing JAK-STAT signaling in a cuprizone-induced demyelination model.

Panax quinquefolius saponins (PQS) were tested in a cuprizone-induced demyelination model to determine how they affect remyelination, lipid metabolism, and JAK-STAT signaling. PQS promoted remyelination by orchestrating the HMGCS1–NPC1–MAL lipid-metabolism axis and rebalancing JAK-STAT pathway activity. This mechanistic evidence positions PQS as a candidate remyelination-promoting therapy for demyelinating diseases such as multiple sclerosis.

Huang J, Sun L, Yue L et al. · Journal of ethnopharmacology · (2026) · View on PubMed ↗

Joint trajectories of ADHD and autistic traits in preschoolers linked to prenatal phthalate exposure: insights from the cord blood metabolome.

Using cord blood metabolomics in 3,083 mother–child pairs, the study examined how prenatal phthalate exposure relates to joint developmental trajectories of ADHD and autistic traits in preschoolers. Specific phthalate metabolites showed time-, sex-, and metabolite-dependent associations, with higher DEHP and high-molecular-weight phthalates linked to increased odds of high-coexistence trajectories. These findings suggest that prenatal exposure to particular phthalates may influence neurodevelopmental risk through metabolome-associated mechanisms.

Yu ZX, Chen HF, Mo HY et al. · Environment international · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 06, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.