PubMed Trending Research Digest — October 12, 2026

Automated digest · 99 articles · 15 research areas · October 12, 2026

Overview

The dominant thread across this week’s papers is precision—using mechanistic biology, high-resolution omics/imaging, and better risk stratification to tailor interventions. In oncology, multiple studies emphasize tumor-ecosystem thinking (immune microenvironment remodeling, spatial niches, and EV-driven metastasis) alongside pathway-targeted strategies (e.g., RAS signaling, Wnt in prostate cancer, and macrophage reprogramming to improve PD-1 blockade). In neurodegeneration and neuroimmunology, work links disease-relevant signaling to actionable targets (gut–brain axis alterations, dopamine-driven innate immune activation via cGAS–STING, and HIV latency control via ENL/USP7/BRD4), while also refining how to measure treatment engagement (regional amyloid PET response heterogeneity).

A second major theme is repurposing and delivery innovation. GLP-1 receptor agonists are repeatedly positioned as multi-system modulators (lung disease and neuroprotection in Parkinson’s), while several studies develop or optimize therapeutic delivery platforms—ranging from inflammation-responsive hydrogels carrying miRNA-loaded sEVs for osteoarthritis, to improved AAV capsids for CNS gene transfer, to engineered regulatory T-cell vesicles for regenerative immunotherapy. Complementing these, multiple guidelines and consensus documents (tinnitus, OSA/CPAP, chronic rhinosinusitis control and sequencing) highlight how evidence is being translated into standardized care pathways.

Finally, several studies reinforce that “real-world” context matters: circadian rhythm disruption associates with metabolic risk, longitudinal CA19-9 trajectories may improve pancreatic cancer surveillance, and pharmacovigilance/algorithmic signal detection improves interpretation of post-withdrawal drug safety. Together, the digest points toward a healthcare future where biomarkers, timing, and patient subtypes—rather than one-size-fits-all approaches—drive both clinical decisions and therapeutic design.

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Infectious Diseases & Antimicrobial Therapy

GLP-1-based therapies in lung diseases.

This review examined the potential of GLP-1 receptor agonists (GLP-1 RAs)—originally developed for type 2 diabetes and obesity—for treatment of chronic lung diseases such as asthma, COPD, pulmonary hypertension, and interstitial lung disease. The key finding is that accumulating evidence supports pleiotropic metabolic and immunomodulatory effects of GLP-1 RAs that may be therapeutically relevant in lung disease pathogenesis and progression. The scientific significance is that GLP-1-based therapies could represent a repurposing opportunity targeting shared inflammatory and vascular mechanisms across multiple chronic respiratory conditions.

O’Callaghan M, Boon MR, Braunstahl GJ et al. · The European respiratory journal · (2026) · View on PubMed ↗

Sputum and oral microbiota profiles are associated with long COVID severity and phenotype post-hospitalisation: a UK multicentre, prospective cohort study.

This UK multicentre prospective cohort study analyzed adults in the PHOSP-COVID study to determine whether oral and sputum microbiota profiles at 6 months post-discharge associate with long COVID severity and phenotype. Using 16S rRNA gene amplicon sequencing and microbiome diversity/co-occurrence network analyses, the authors report that sputum and oral microbiota signatures correlate with long COVID severity clusters and symptom subgroups, linking microbial patterns to inflammation. Clinically, these microbiota associations may help stratify long COVID phenotypes and identify potential inflammatory targets for future interventions.

Alferes de Lima Headley D, Richardson H, Hennayake C et al. · The European respiratory journal · (2026) · View on PubMed ↗

ERS/ESRS clinical practice guideline for continuous positive airway pressure for the treatment of adult obstructive sleep apnoea.

This ERS/ESRS clinical practice guideline evaluated continuous positive airway pressure (CPAP) for adult obstructive sleep apnoea (OSA), comparing CPAP with no or sham treatment across OSA subgroups. The key finding is that the guideline assesses CPAP’s effects on patient-centered and prognostically relevant outcomes and emphasizes differential effectiveness by OSA subtype. Scientifically and clinically, it provides evidence-based recommendations to optimize CPAP use and improve outcomes in adult OSA populations.

Testelmans D, Schwarz EI, Anttalainen U et al. · The European respiratory journal · (2026) · View on PubMed ↗

Blockade of mutant RAS oncogenic signaling: a 2026 update.

This pharmacology update reviewed the molecular basis and therapeutic strategies for blocking mutant RAS oncogenic signaling across cancers, with emphasis on KRAS as the most frequently mutated RAS isoform. The key finding is that effective RAS pathway inhibition can target multiple nodes in the RAS-GTP signaling network (including upstream regulators like GEFs and downstream effectors such as RAF-MEK-ERK and PI3K-AKT), reflecting the central role of RAS cycling between GDP and GTP states. The clinical significance is that it frames current and emerging drug approaches for RAS-driven malignancies, supporting rational selection of pathway-targeted therapies.

Roskoski R · Pharmacological research · (2026) · View on PubMed ↗

Strengthening health systems to prioritise, provide care, and prevent osteoarthritis: a roadmap for global health policy.

This Lancet policy roadmap studied how global health systems can prioritize, provide care, and prevent osteoarthritis, focusing on the mismatch between the disease burden and its visibility in national and global agendas. The key finding is that osteoarthritis “identity problems” (stigma, inequities, and fragmented service integration) contribute to deprioritization and limited access to effective interventions. The scientific and policy significance is that it proposes actionable strategies to strengthen osteoarthritis inclusion in health systems to reduce disability for the projected near-1-billion global burden by 2050.

Briggs AM, Bowden JL, Risberg MA et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Emerging novel therapies for the treatment of hereditary haemorrhagic telangiectasia.

This review article examined emerging novel therapies for hereditary haemorrhagic telangiectasia (HHT), an autosomal dominant vasculopathy driven by dysregulated angiogenic signaling. The key finding is that new treatment approaches are being developed to address major HHT complications such as chronic epistaxis, gastrointestinal bleeding, iron deficiency anemia, and high-risk intracranial haemorrhage. Clinically, it highlights evolving therapeutic options that could reduce morbidity in HHT patients, including women who experience substantial disease burden.

Al-Samkari H · The Lancet. Haematology · (2026) · View on PubMed ↗

Reference frame for Adult Brainstem gliomas.

This article proposed a reference framework for adult brainstem gliomas (BSG), a rare adult tumor subtype with heterogeneous outcomes and important differential diagnoses. The key finding is that standardized clinical decision-making should guide tissue sampling and surgical approach selection among stereotactic biopsy, open biopsy, and resection, with emphasis on enabling histomolecular analyses to confirm diagnosis and subtype. Scientifically, it supports more consistent diagnostic workflows that improve the accuracy of molecular classification and downstream management for adult BSG.

Laigle-Donadey F, Mesny E, Bielle F et al. · The oncologist · (2026) · View on PubMed ↗

Prominent V Waves Augment Right Ventricular Afterload Independent of the Lung Vessels in Heart Failure: Implications for Clinical Assessment of Pulmonary Vascular Disease.

This retrospective cohort study investigated heart failure with preserved ejection fraction (HFpEF) patients to determine whether prominent V waves reflect right ventricular afterload independent of lung vessels. Using invasive hemodynamic exercise testing, the authors defined heightened left atrial (LA) stiffening by a pulmonary artery wedge pressure (PAWP) V wave exceeding mean PAWP by ≥10 mm Hg and found that prominent V waves augment right ventricular afterload beyond effects attributable to lung vasculature. Clinically, this supports using V-wave–based hemodynamic assessment to better identify pulmonary vascular disease mechanisms and refine evaluation in HFpEF.

Chaikijurajai T, Reddy YNV, Harada T et al. · Circulation · (2026) · View on PubMed ↗

Maternal smoking and risk of childhood cancer: a report from the Childhood Cancer and Leukemia International Consortium.

This multinational analysis studied whether maternal prenatal smoking is associated with childhood cancer risk using prospectively recorded, population-based case-control record-linkage data from the Childhood Cancer and Leukemia International Consortium. Using probabilistic bias methods to address bias from prior case-control designs, the study clarified the nature of the maternal smoking–childhood cancer relationship rather than relying on potentially biased retrospective comparisons. The findings are significant for refining causal inference about prenatal tobacco exposure as a modifiable risk factor for childhood malignancy.

Domingues A, Spector LG, Tettamanti G et al. · International journal of epidemiology · (2026) · View on PubMed ↗ · Free PDF ↗

Golgi disassembly: a key process for autophagy-mediated regulation of oocyte spindle migration.

This study investigated Golgi disassembly during oocyte meiosis I and its role in spindle cortical migration in oocytes, focusing on timing around germinal vesicle breakdown (GVBD) through metaphase II (MII). It found that Golgi vesiculation peaks at GVBD and is largely completed by MII, and that—unlike mitosis—the vesiculation stage regulates spindle cortical migration during metaphase I (MI) to establish oocyte polarity. These results are significant for understanding the cell-biological mechanisms that ensure correct meiotic spindle positioning and polarity in human/animal reproduction.

Zhang J, Wang N, Wang X et al. · Autophagy · (2026) · View on PubMed ↗

Pregnancy Complicated by Citrin Deficiency and Gestational Diabetes Mellitus: Perioperative Metabolic Management and Postoperative Analgesic Challenges Following Caesarean Delivery.

This case report described perioperative metabolic management and postoperative analgesic challenges in a 25-year-old pregnant woman with genetically confirmed citrin deficiency due to an SLC25A13 c.1763G>A homozygous mutation complicated by gestational diabetes mellitus (GDM). The report highlights the need to coordinate obstetric care with inherited metabolic disease requirements while managing severe first-trimester nausea/vomiting and later GDM diagnosed via capillary glucose testing. Scientifically and clinically, it underscores how rare SLC25A13-related metabolic disorders can complicate pregnancy and perioperative planning, including analgesic considerations after cesarean delivery.

Naing EEP, Kyaw EMM · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

Neuromuscular, Balance, and Gait Factors Associated with Falls and Fall-Related Outcomes in Individuals with COPD: A Systematic Review.

This systematic review synthesized evidence on neuromuscular, balance, and gait factors associated with falls and fall-related outcomes in individuals with COPD, including 25 original studies totaling 1295 participants. It assessed relationships between impairments in muscle strength, balance, and gait and subsequent falls or related outcomes using literature searches through November 2024. The significance is that it helps identify modifiable physical risk domains for fall prevention strategies in COPD populations.

Zangi M, Shamsi H, Rahmani Rasa A et al. · International journal of chronic obstructive pulmonary disease · (2026) · View on PubMed ↗ · Free PDF ↗

Endothelial Dysfunction and Metabolic Reprogramming in Cardiovascular Diseases.

This review article examined how endothelial dysfunction in cardiovascular diseases is driven by metabolic reprogramming in endothelial cells under conditions such as hypertension, hyperglycemia, and hyperlipidemia. It reports that altered metabolic pathway usage (shifts among glycolysis, fatty acid oxidation, and amino acid metabolism) contributes to reduced nitric oxide (NO), increased oxidative stress/inflammation, and impaired vascular barrier integrity, accelerating atherosclerosis, myocardial infarction, calcific aortic valve disease, and aortic aneurysms. The scientific significance is that it frames endothelial metabolic pathways as mechanistic targets for future cardiovascular therapies.

Chen H, Zhao Y, Ge C et al. · Reviews in cardiovascular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Early Initiation of Sodium-Glucose Cotransporter 2 Inhibitors in Acute Decompensated Heart Failure: Efficacy, Safety, and Implementation in Stabilized Patients.

This narrative review evaluated early in-hospital initiation of sodium-glucose cotransporter 2 (SGLT2) inhibitors in patients with acute decompensated heart failure (ADHF) after stabilization in ICU/CCU settings. It summarizes emerging clinical evidence on efficacy, safety, and implementation concerns—particularly hemodynamic stability and renal function—when starting SGLT2 inhibitors during the vulnerable acute phase. The significance is that it supports evidence-based protocols for earlier disease-modifying therapy in ADHF rather than delaying initiation until after discharge.

Mauriello A, Correra A, Maratea AC et al. · Reviews in cardiovascular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Physical Activity, Myokine-Adipokine Signatures and Haemoglobin Glycation Index in Adults with Type 2 Diabetes.

This cross-sectional study in 185 adults with type 2 diabetes examined associations between hemoglobin glycation index (HGI) and circulating myokines (irisin, myostatin, myonectin, IL-6, IL-15) and adipokines (leptin, adiponectin), testing whether relationships differ by physical activity status and exercise modality. It focused on HGI as a marker of metabolic heterogeneity and cardiovascular risk beyond ambient glycemia and analyzed how exercise-related biomarker patterns relate to glycation variability. The clinical significance is that identifying myokine/adipokine signatures linked to HGI could help stratify cardiometabolic risk and tailor lifestyle or therapeutic approaches in T2DM.

Ismail M, Ibrahim Hassan M, Shahzoda Fozilovna A et al. · Diabetes, metabolic syndrome and obesity : targets and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Severe Euglycemic Diabetic Ketoacidosis After Semaglutide-Associated Poor Intake Despite Empagliflozin Discontinuation: A Case Report.

This case report described severe euglycemic diabetic ketoacidosis (EDKA) in a 68-year-old woman with type 2 diabetes after semaglutide-associated poor oral intake despite discontinuing empagliflozin. The patient developed nausea, vomiting, and diarrhea with minimal intake after starting semaglutide (0.25 mg weekly then 0.5 mg weekly), and medication reconciliation indicated empagliflozin, metformin, and pioglitazone were stopped about two weeks before presentation while semaglutide continued. The clinical significance is that semaglutide plus reduced intake can precipitate EDKA even when SGLT2 inhibitor therapy has been stopped, emphasizing the need for vigilance for ketoacidosis in “near-normal glucose” presentations.

Niknam K, Niknam T · International medical case reports journal · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of Perioperative Intravenous Lidocaine on Rebound Pain After Interscalene Brachial Plexus Block for Arthroscopic Rotator Cuff Repair: A Randomized Placebo-Controlled Trial.

This single-center randomized, placebo-controlled Phase II trial studied whether perioperative intravenous lidocaine reduces rebound pain within 24 hours after single-shot interscalene brachial plexus block for arthroscopic rotator cuff repair in 120 adults. Participants received either saline or lidocaine (1 mg/kg loading dose before induction followed by 2 mg·kg−1·h−1 from skin incision to closure), with rebound pain as the primary outcome. The significance is that it tests a practical perioperative pharmacologic strategy to preserve early analgesic benefit from regional anesthesia by mitigating rebound pain after shoulder surgery.

Zhang B, Liu Y, Zheng J · Drug design, development and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Recent advances in antituberculosis drugs and therapeutics: from mechanistic breakthroughs to clinical translation.

This review synthesized 2020–2025 anti-tuberculosis drug and therapeutics advances, focusing on mechanism-driven strategies for Mycobacterium tuberculosis in the context of drug-resistant TB, adult BCG limitations, and treatment gaps. It reports that integrating structural biology, multi-omics, and real-world clinical evidence is enabling more precision-oriented therapeutic development and translation. These advances are clinically significant because they aim to improve outcomes in drug-resistant TB and accelerate effective new regimens for vulnerable populations.

Pan Z, Liu G, Li Y et al. · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Prolonged tadalafil exposure promotes skeletal muscle myogenesis and regulates early myogenic markers activation in C2C12 cell lines.

This in vitro study tested whether prolonged exposure to tadalafil, a phosphodiesterase type 5 inhibitor, affects skeletal muscle myogenesis in C2C12 mouse myoblast cell lines. Treatment with 1 µM tadalafil for up to seven days increased proliferation and promoted early myogenic marker activation, alongside changes in myokine release. The findings are significant because they suggest tadalafil may modulate nitric oxide/cGMP-linked pathways that regulate myogenic progression, informing potential therapeutic strategies for muscle regeneration.

Antinozzi C, Di Luigi L · Molecular biology reports · (2026) · View on PubMed ↗

Disproportionality Analysis of FAERS Data Divergence and a Systematic Review of Comparative Safety Studies: Lessons Learned from the Example of Ranitidine and Cancer Risk.

This pharmacovigilance study evaluated ranitidine-associated cancer signals using disproportionality analysis of FAERS and JADER databases, complemented by a systematic review of comparative safety studies. It applied four complementary signal-detection algorithms (including PRR and related methods) to assess whether ranitidine signals for cancer risk diverged across databases and how bias-mitigation approaches performed. The clinical significance is improved interpretation of post-withdrawal safety signals for ranitidine and guidance on more reliable comparative safety assessment using real-world adverse event data.

Rathod M, Kadari M, Mohan HR et al. · Drug safety · (2026) · View on PubMed ↗

Multi-carbapenemase-producing Klebsiella pneumoniae: Genomic characterization and In Vitro evaluation of cefiderocol and novel β-lactam/β-lactamase inhibitor combinations.

This study characterized multi-carbapenemase-producing Klebsiella pneumoniae isolates from bloodstream infections in 14 Italian hospitals (2022–2023) and tested in vitro activity of cefiderocol and novel β-lactam/β-lactamase inhibitor combinations. It reports genomic/epidemiologic characterization of MCP-Kp and susceptibility testing results against agents including cefiderocol, aztreonam/avibactam, cefepime/zidebactam, and cefepime/enmetazobactam. The scientific and clinical significance is identifying which newer antimicrobials retain activity against highly resistant MCP-Kp, supporting treatment options for severe bloodstream infections.

Cornacchia A, Comini S, Pomilio F et al. · Molecular biology reports · (2026) · View on PubMed ↗

PTK7 scaffolds DNA-PKcs to promote DNA damage response and immune evasion in triple-negative breast cancer.

This study investigated the intracellular role of the pseudokinase PTK7 in triple-negative breast cancer (TNBC) cells and tumors, focusing on how PTK7 affects DNA damage response and immune evasion. PTK7 translocated to the nucleus and scaffolded DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to enhance its activation and promote non-homologous end joining (NHEJ) repair, with PTK7 loss impairing these processes. These findings suggest PTK7–DNA-PKcs axis targeting could both sensitize TNBC to DNA damage and reduce tumor immune escape.

Liu X, Zhang K, Zhang Y et al. · Oncogene · (2026) · View on PubMed ↗

Canonical Wnt signaling in the regulation of prostate cancer stem cells: a key driver of castration-resistant prostate cancer and a therapeutic opportunity.

This review examined how canonical Wnt signaling regulates prostate cancer stem cells (PCSCs) and thereby drives castration-resistant prostate cancer (CRPC) progression and therapeutic resistance in men with prostate cancer. It highlights aberrant canonical Wnt pathway activation as a key regulator of PCSC self-renewal, lineage plasticity, epithelial–mesenchymal transition (EMT), and bone metastatic capacity, framing Wnt signaling as a therapeutic opportunity. Clinically, the synthesis supports Wnt-pathway modulation as a strategy to prevent or treat CRPC by disrupting PCSC-driven relapse.

Li H, Xu H, Hou Y et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Decoding the cholangiocarcinoma tumor microenvironment: from single-cell and spatial atlases to translational therapeutic targeting.

This article reviewed how the cholangiocarcinoma tumor microenvironment is characterized using single-cell and spatial atlases (single-cell RNA-seq, multi-omics, spatial transcriptomics/proteomics, multiplex imaging, and pathomics) and how these data can be translated into therapeutic targeting. It emphasizes that CCA progression and treatment failure are not explained solely by tumor-cell intrinsic genomic alterations, but instead reflect an ecosystem of malignant cholangiocytes interacting with stromal and immune components. The work supports atlas-guided, microenvironment-directed therapeutic development to overcome resistance to chemotherapy, immunotherapy, and targeted agents.

Zhang L, Zhang K, Xue J et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Utility of longitudinal changes in CA19-9 for detection of pancreatic ductal adenocarcinoma in patients with benign pancreatic diseases.

This retrospective study evaluated whether longitudinal changes in carbohydrate antigen 19-9 (CA19-9) improve early detection of pancreatic ductal adenocarcinoma (PDAC) among 656 patients with benign pancreatic diseases (pancreatic cysts, intraductal papillary mucinous neoplasms, chronic pancreatitis, and autoimmune pancreatitis). Patients were classified as PDAC (n=34) versus controls (n=622), and the study assessed CA19-9 absolute-value trajectories and related metrics over follow-up. If validated, longitudinal CA19-9 dynamics could refine surveillance and enable earlier PDAC detection in high-risk benign pancreatic disease populations.

Abe T, Takikawa T, Kikuta K et al. · Pancreatology : official journal of the International Association of Pancreatology (IAP) … [et al.] · (2026) · View on PubMed ↗

A GLP-1/apelin dual receptor agonist shows neuroprotective effects in the MPTP mouse model of Parkinson’s disease.

This preclinical study tested a rationally designed bifunctional peptide, ELA (exendin-4-linker-apelin), in the MPTP mouse model of Parkinson’s disease, using the GLP-1 receptor agonist liraglutide as a comparator. ELA improved motor performance in behavioral assays (open field, pole test, rotarod) and showed anti-inflammatory effects alongside neuroprotection relative to controls. These results support GLP-1/APJ dual-receptor agonism as a potential disease-modifying therapeutic approach for Parkinson’s disease.

Xu A, Wei Y, Liu E et al. · Biochemical pharmacology · (2026) · View on PubMed ↗

NuPath, a higher-sensitivity TRUPATH-derived biosensor, expands detection of basal and agonist-induced GPCR activation.

This engineering study developed NuPath, a higher-sensitivity TRUPATH-derived bioluminescence resonance energy transfer (BRET) biosensor, to quantify basal and agonist-induced heterotrimeric G protein activation downstream of GPCRs. By substituting RLuc8 in Gα with NanoLuc (nLuc) and replacing GFP2 with eYFP fused to Gγ while preserving sensor architecture, NuPath expanded dynamic range and improved detection of subtle or constitutively active signaling in a 96-well plate format. The improved biosensor sensitivity can accelerate GPCR pharmacology by enabling more precise measurement of G protein activation states.

Dehkhoda F, Misganaw D, Montenegro E et al. · Biochemical pharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

“Ozempic Face” and Facial Aging.

This narrative review addressed the clinical phenomenon of “Ozempic face,” describing facial aging changes associated with rapid weight loss in patients using GLP-1 receptor agonists such as semaglutide (Ozempic). It summarizes anatomical and histological mechanisms including dermal white adipose tissue (dWAT) volume loss, skeletal remodeling, and sarcopenia that contribute to volume deflation, skin laxity, and reduced structural support. The review is clinically significant for guiding dermatologic and cosmetic management of GLP-1–associated facial changes.

Fathizadeh S, Hwang AS, Hoss E · Clinics in dermatology · (2026) · View on PubMed ↗ · Free PDF ↗

Partial convergence of alternative polyadenylation changes across ALS-Associated RNA-Binding proteins.

This study analyzed whether alternative polyadenylation (APA) changes converge across multiple ALS-associated RNA-binding proteins by comparing poly(A)-site usage after TDP-43 knockdown, TDP-43 K263E expression, FUS knockout, FUS P525L expression, and MATR3 knockout. It found that APA effects varied substantially by dataset, with FUS knockout producing the strongest response (373 significant events across 239 genes) and only a small number of events showing partial overlap across conditions. These results suggest limited shared APA dysregulation among ALS RNA-binding protein perturbations, informing how transcript 3′-end remodeling may differ by genetic driver.

Ji C · Neuroscience · (2026) · View on PubMed ↗

Androgen receptor-regulated ZNF419 modulates ferroptosis sensitivity via the ZDHHC20-GPX4 pathway in prostate cancer.

This study investigated how androgen receptor (AR) signaling regulates ferroptosis sensitivity in prostate cancer via the AR-regulated zinc finger gene ZNF419 and the ZDHHC20–GPX4 pathway. It found that ZNF419 expression is elevated in prostate cancer, correlates with poor outcomes, and reduces ferroptosis susceptibility, with promoter-proximal AR occupancy at predicted androgen response elements supporting transcriptional regulation. Mechanistically, the AR–ZNF419 axis modulating ZDHHC20–GPX4 provides a potential target to sensitize prostate tumors to ferroptosis-based therapies.

Hou Y, Zhao W, Liu J et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗

Lysosomal Competence in Skeletal Muscle Aging: Autophagic Flux, Measurement Gaps, and Human Translation.

This narrative review examined lysosomal competence in skeletal muscle aging, focusing on autophagic flux measurement, lysosomal acidification/degradative capacity, and how these relate to sarcopenia and translational gaps to human disease. It argues that evidence from different aging contexts (healthy aging, frailty, disuse, cachexia, obesity, chronic disease) should not be treated as interchangeable and evaluates where experimental-to-human translation is strong versus limited. Scientifically, clarifying lysosome–autophagy dynamics and measurement pitfalls could improve biomarkers and therapeutic targeting for age-related muscle decline.

Dogsom O, Kim JG, Lee YH et al. · Aging and disease · (2026) · View on PubMed ↗ · Free PDF ↗

Tissue-Specific Isolation of Hepatocyte Extracellular Vesicles From Human Plasma Enables Tissue-Resolved Proteomic and miRNA Profiling.

The study developed NEXPLOR, an immunoaffinity platform to selectively isolate liver-derived hepatocyte extracellular vesicles (hepatocyte-EVs) from human plasma using a four-marker antibody panel (ASGR1, ASGR2, TFR2, SLCO1B1). In a clinical cohort including hepatocellular carcinoma (HCC) and non-cancer cirrhosis, the approach enabled tissue-resolved proteomic and miRNA profiling while avoiding co-capture of the dominant platelet- and leukocyte-EV background. This improves liquid biopsy precision by enabling liver-tissue EV biomarker discovery and monitoring in liver disease and cancer.

Figueiras R, Vagueiro S, Kay R et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗ · Free PDF ↗

M2 Macrophage-Derived Small Extracellular Vesicle miR-106a-Loaded QCG Hydrogel Targets the RNF128-LXR Pathway to Reprogram Chondrocyte Cholesterol Metabolism for Osteoarthritis Therapy.

The study engineered an inflammation-responsive injectable QCG hydrogel (quaternized chitosan plus CPBA-gelatin) to locally deliver miR-106a-loaded small extracellular vesicles (sEVs) derived from M2 macrophages to treat osteoarthritis in relevant models. QCG@sEV-miR-106a reprogrammed chondrocyte cholesterol metabolism by targeting the RNF128–LXR pathway, with sEV identity confirmed by transmission electron microscopy, nanoparticle tracking analysis, and vesicle marker profiling. This suggests a macrophage-EV/miRNA therapeutic strategy that couples local biomaterial delivery with pathway-specific metabolic reprogramming for OA.

Liu B, Wang Z, Zhang J et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗ · Free PDF ↗

MVB Maturation Responsive to KRASG12D/TP53R175H Co-mutations Fuels Extracellular Vesicle-hypersecretion Phenotype to Aggravate Lymphangiogenesis and Lymphatic Metastasis.

The study investigated how KRASG12D/TP53R175H co-mutations drive lymphangiogenesis and lymphatic metastasis using KRASG12D/TP53R175H-related orthotopic xenograft models and multi-center patient cohorts. It found that KRASG12D-mediated phosphorylation of TP53R175H promotes FUS transcriptional activation, leading to an extracellular vesicle hypersecretion phenotype that aggravates lymphangiogenesis and lymph node metastasis. This links specific oncogenic co-mutations to a mechanistic EV-driven metastatic program, identifying FUS and EV hypersecretion as potential therapeutic targets.

Yang J, Luo Y, Zhou Y et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗ · Free PDF ↗

Cerebriform Nests on Reflectance Confocal Microscopy: Bridging Architecture, Tumor Biology, and Prognosis in Melanoma- a systematic review.

This systematic review evaluated reflectance confocal microscopy (RCM) evidence for “cerebriform nests” in melanoma and how this RCM architecture correlates with histopathology, molecular features, and prognosis. It summarizes the defining RCM pattern (multilobulated dermal aggregates with convoluted, brain-like contours and heterogeneous reflectivity) and the reported clinical associations across included studies. Clinically, it supports RCM cerebriform-nest recognition as a noninvasive imaging biomarker candidate for melanoma risk stratification and diagnostic refinement.

Alma A, Gherbassi S, Clementi A et al. · Dermatology (Basel, Switzerland) · (2026) · View on PubMed ↗

Surgery and/or biologics in chronic rhinosinusitis with nasal polyps: EUFOREA/EPOS consensus paper.

This EUFOREA/EPOS consensus paper reviewed evidence on sequencing and positioning of endoscopic sinus surgery (ESS) and biologics for chronic rhinosinusitis with nasal polyps (CRSwNP). It provides expert recommendations on aims, indications, timing, and how to integrate ESS with biologic therapy based on pivotal randomized trials, real-world studies, and recent guidelines. The significance is improved standardized decision-making for optimizing treatment order and extent in CRSwNP patients receiving biologics.

de Corso E, Hellings PW, Fokkens WJ et al. · Rhinology · (2026) · View on PubMed ↗

Pectin alleviates alcohol-associated liver disease partly through cell-type-specific aryl hydrocarbon receptor signaling in female mice.

The study tested whether pectin alleviates alcohol-associated liver disease (ALD) through cell-type-specific aryl hydrocarbon receptor (AhR) signaling in female mice using conditional AhR knockout models in intestinal epithelial cells, hepatocytes, dendritic cells, and Rorγt-positive cells. Using the Lieber–DeCarli ALD model with pectin supplementation, it found that AhR deficiency in specific compartments (notably intestinal epithelial cells and hepatocytes) reduced pectin’s protective effects, implicating gut-liver axis AhR signaling in ALD. This supports a mechanistic basis for pectin as a therapy that acts via compartmentalized AhR pathways rather than a single systemic target.

Hu W, Schlecht-Louf G, Vielhescaze C et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Dopamine-induced mitochondrial dysfunction activates cGAS-sTING to drive IL-6 secretion in macrophages.

The study defined how dopamine triggers IL-6 secretion in primary human monocyte-derived macrophages (hMDMs) via mitochondrial dysfunction and innate immune sensing. Dopamine caused transient mitochondrial membrane depolarization and sustained changes in mitochondrial dynamics/metabolism, leading to cytosolic mtDNA release that activated the cGAS–STING pathway and NF-κB signaling. This mechanistically connects dopamine exposure to macrophage inflammatory cytokine production, highlighting cGAS–STING as a potential intervention point.

Daniali M, Channer B, Curley EO et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

The ENL-USP7 complex regulates HIV latency through BRD4 protein stabilization.

The study investigated host mechanisms maintaining HIV latency in CD4+ T cells and brain microglia by identifying an ENL–USP7 complex that stabilizes BRD4. It showed that pharmacologic inhibition or genetic loss of ENL reactivated latent HIV, and that USP7 maintained BRD4 protein stability; targeted USP7 degradation using a PROTAC induced latency reversal and destabilized BRD4. This provides a druggable latency-control axis (ENL/USP7/BRD4) for strategies aiming to reactivate and potentially eliminate latent HIV.

Ahmed W, Li X, Shabangu CS et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Oxidative DNA damage drives centromere fragility and chromosome instability.

The study examined how oxidative DNA damage affects centromere integrity and chromosome stability by using a chemoptogenetic system to generate singlet oxygen locally at centromeres. It found that centromeric oxidative base lesions slow DNA synthesis, destabilize CENP-A chromatin, and create DNA breaks that persist into subsequent cell cycles, producing chromosome instability. Scientifically, it clarifies a direct causal pathway from localized oxidative damage to centromere fragility, informing cancer biology and potential vulnerability targeting.

Thompson L, Nassar R, Angrisani A et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

New CRS control tests: development and validation by EUFOREA.

The study developed and validated two new chronic rhinosinusitis (CRS) control instruments—the 6-item CRS Control Test (CCT) and the 14-item CRS Patient Control Test (CPCT)—through the EUFOREA initiative. In a survey of 1,102 CRS patients across 19 centers in 7 countries, the new tests showed convergent and discriminative validity and correlated with established measures including EPOS control test, VAS severity, SNOT-22, and PGAT. This provides improved, standardized tools to quantify CRS control for clinical evaluation and research.

Conti DM, Fokkens WJ, Scadding GK et al. · Rhinology · (2026) · View on PubMed ↗

PKP2 orchestrates OXPHOS expression in cardiomyocytes via a PGC1α-dependent mechanism.

This study examined how plakophilin-2 (PKP2) mutations affect mitochondrial oxidative phosphorylation (OXPHOS) gene expression in PKP2 mutant human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and in myocardial tissue from arrhythmogenic cardiomyopathy (ACM) patients. Transcriptomic profiling showed consistent downregulation of OXPHOS genes in PKP2 mutant hiPSC-CMs, and the authors report that PKP2 regulates OXPHOS through a PGC1α-dependent mechanism. These findings link desmosomal dysfunction to impaired mitochondrial energy programs, suggesting PGC1α/OXPHOS pathways as potential targets to modify ACM progression, including exercise-related disease mechanisms.

Han SJ, van den Berg D, de Ruiter H et al. · Cardiovascular research · (2026) · View on PubMed ↗ · Free PDF ↗

Fanconi anemia pathway disruption drives lomustine sensitivity in glioma.

This study investigated determinants of glioma sensitivity to the nitrosourea lomustine (CCNU) by performing CRISPR-Cas9 genome-wide functional knockout screening in experimental glioma models and validating hits in an immunocompetent glioma mouse model using RCAS/tv-a somatic gene delivery. The key finding is that disruption of Fanconi anemia (FA) pathway genes drives lomustine sensitivity, indicating a synthetic lethal relationship between CCNU treatment and FA pathway integrity. Clinically, this supports FA pathway status as a potential biomarker for CCNU responsiveness and provides mechanistic rationale for combination strategies that exploit FA pathway vulnerabilities in glioblastoma.

Becker H, Walter B, Haeusser LA et al. · Neuro-oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Perioperative Myocardial Injury and Infarction: Thrombotic Mechanisms, Diagnostic Challenges, and Antithrombotic Management.

This narrative review synthesized evidence on perioperative myocardial injury (PMI) and perioperative myocardial infarction (PMIn) after noncardiac surgery, focusing on thrombotic mechanisms, diagnostic challenges, and antithrombotic management. The authors highlight that surgical stress promotes a prothrombotic milieu involving platelet activation, coagulation amplification, impaired fibrinolysis, endothelial dysfunction, and plaque destabilization, which complicates diagnosis because many events are clinically silent. The review’s significance is to guide risk stratification and management—particularly using coronary computed tomography angiography (CCTA) and thrombogenicity biomarkers—to improve outcomes after surgery.

Jang JY, Bae JS, Cho YH et al. · Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · (2026) · View on PubMed ↗ · Free PDF ↗

Rare Coding Variants in FOXF1 are Associated with Pulmonary Arterial Hypertension.

This study assessed whether rare coding variants in the transcription factor FOXF1 contribute to pulmonary arterial hypertension (PAH) by identifying ultra-rare missense FOXF1 variants in two index cases and evaluating FOXF1 frequency, expression, and functional relevance across three independent international PAH cohorts. The key finding is an association between rare FOXF1 missense variants and PAH, consistent with FOXF1’s role in lung vascular development. Scientifically and clinically, the results expand the genetic architecture of nonheritable PAH and support FOXF1 variant screening and functional follow-up as steps toward improved molecular diagnosis.

Gomez-Arroyo J, Houweling AC, Postma AV et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗

Spatial transcriptomics elucidates trajectories associated with transformation in malignant peripheral nerve sheath tumors.

This study used spatial transcriptomics to map tumor microenvironment niches and infer trajectories of malignant transformation in malignant peripheral nerve sheath tumors (MPNSTs), integrating deep learning image analysis with 50,896 transcriptomes from 15 human MPNSTs. The key finding is that spatially resolved gene expression trajectories link genetic alterations with immune microenvironment features and local invasion/transformation patterns within tumors. This is significant because it provides a framework for understanding intra-tumor heterogeneity in MPNSTs and may inform more precise diagnostic classification and spatially targeted therapeutic strategies.

Mirchia K, Bhattacharya A, Viken JK et al. · Neuro-oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of evolocumab on lipid profile and circulating endothelial biomarkers in patients undergoing primary percutaneous coronary intervention.

This single-center, open-label randomized trial evaluated whether early addition of the PCSK9 inhibitor evolocumab to atorvastatin improves lipid profiles and circulating endothelial biomarkers in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). The key finding is that evolocumab plus atorvastatin (140 mg biweekly) for 12 weeks favorably modulated lipid metabolism and circulating endothelial/inflammatory biomarkers compared with atorvastatin alone. Clinically, these results support early PCSK9 inhibition as a strategy to improve vascular biology after PPCI, potentially contributing to better post-MI risk reduction.

Jiang W, Liu M, Xiong X et al. · Science progress · (2026) · View on PubMed ↗ · Free PDF ↗

Guideline-Directed Treatment Eligibility and Burden of Untreated Stage-1 Hypertension Under the 2025 American College of Cardiology/American Heart Association Hypertension Guideline: Insights From NHANES 2015 to 2020.

This cross-sectional analysis used NHANES 2015–2020 data to quantify how guideline-directed treatment eligibility changes for adults with untreated stage 1 hypertension under the 2025 ACC/AHA hypertension guideline using the Predicting Risk of Cardiovascular Disease Events (PCE) risk model versus the 2017 pooled cohort equations. The key finding is that adopting the PCE-based 2025 framework reclassifies the number and characteristics of adults recommended for treatment compared with the prior 2017 approach. The significance is that it informs clinicians and health systems about the expected burden of untreated stage 1 hypertension management under updated risk prediction criteria.

Jian Q, Chen Y, Ruzieh M et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

The effect of Red Bull energy drink on strength, power, and jump performance in female volleyball players: A randomized cross-over trial.

This randomized, double-blind, placebo-controlled crossover trial tested whether acute ingestion of a standard Red Bull energy drink serving affects anaerobic power, handgrip strength, and jump performance in 15 female sub-elite volleyball players. The key finding is whether Red Bull produces measurable short-term improvements in these performance outcomes compared with placebo under controlled conditions. If positive, the results would clarify the ergogenic potential of commercially available energy drinks (caffeine/taurine) for female volleyball performance; if null, they would argue against expecting meaningful acute benefits.

Harrisová HE, Bahenský P, Mrkvička T et al. · Nutrition and health · (2026) · View on PubMed ↗

USP11 Drives Cerebral Ischemia-Reperfusion Injury Via Promoting Ferroptosis by Deubiquitinating and Stabilizing ASK1.

This study investigated the role of ubiquitin-specific protease 11 (USP11) in cerebral ischemia-reperfusion injury (CIRI) by using USP11 knockout (USP11-KO) and adeno-associated virus–mediated modulation in models of ischemia-reperfusion. The key finding is that USP11 promotes ferroptosis in CIRI by deubiquitinating and stabilizing apoptosis signal-regulating kinase 1 (ASK1). Scientifically, this identifies a USP11–ASK1–ferroptosis axis as a mechanistic driver of CIRI and suggests USP11 inhibition as a potential therapeutic strategy to prevent or treat ischemic stroke injury.

Hu S, Wang K, He M et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

Preconception incretin therapy reduces pregnancy and cardiometabolic outcomes in polycystic ovary syndrome.

This study used a target trial emulation in women with polycystic ovary syndrome/polyendocrine metabolic ovarian syndrome (PCOS/PMOS) within the TriNetX federated network to compare preconception GLP-1/dual GLP-1/GIP receptor agonist therapy (liraglutide, semaglutide, or tirzepatide) versus metformin. Preconception incretin therapy was associated with reduced pregnancy and cardiometabolic adverse outcomes after propensity score matching (1:1). These findings support using GLP-1–based incretin receptor agonists as a potentially safer preconception strategy to improve both reproductive and metabolic trajectories in PCOS/PMOS.

Henney AE, Holmes PJ, Riley D et al. · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Inducible dCas12a system expands CRISPRi/a capabilities for functional genomics in malaria parasite Plasmodium falciparum.

Researchers developed an inducible dead Cas12a (dCas12a) CRISPR interference/activation (CRISPRi/a) platform for functional genomics in the malaria parasite Plasmodium falciparum. Unlike dCas9 systems constrained by NGG PAMs, dCas12a recognizes T-rich PAMs and can process one transcript into multiple sgRNAs, enabling multiplexed gene regulation, with functional validation targeting EBA175 and ATG18. This expands the CRISPRi/a toolkit for P. falciparum and improves the ability to interrogate gene function and pathways relevant to malaria biology.

Lucky AB, Li X, Kobakhidze G et al. · iScience · (2026) · View on PubMed ↗ · Free PDF ↗

Seven-day versus fourteen-day low-dose primaquine for Plasmodium vivax malaria in India: an open-label, non-inferiority, randomised, controlled trial.

This open-label, non-inferiority randomized controlled trial enrolled adults (>16 years) in India with microscopically confirmed Plasmodium vivax mono-infection and normal G6PD activity to compare primaquine 3.5 mg/kg total dose given over 7 days versus the standard 14-day regimen. The 7-day low-dose schedule was tested for comparable efficacy and safety for preventing relapse while addressing poor adherence with the longer course. If non-inferiority is confirmed, the shorter primaquine regimen could improve real-world adherence and reduce P. vivax relapse burden in India.

Baharia RK, Singh-Phulgenda S, Naser SM et al. · The Lancet regional health. Southeast Asia · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

Machine Learning-Based Prediction of Mortality in Patients With Mitral Regurgitation: Results From Two Nationwide, Prospective Studies.

Using two nationwide prospective cohorts, investigators built and externally validated a machine learning model to predict mortality in patients with significant mitral regurgitation from the ChinaValvular Heart Disease (China-VHD) registry and an external China cohort. The final model combined feature selection approaches (Cox stepwise regression, LASSO-penalized Cox regression, and Boruta) and outperformed multiple comparator models in internal and external validation. Clinically, this provides a data-driven risk stratification tool to support prognosis and potentially guide management decisions in MR patients.

Yin Y, Lv J, Zhao Q et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

Regional amyloid-PET clearance dynamics and anti-Aβ monoclonal antibody therapy: a preliminary real-world study.

In a real-world longitudinal study, 26 patients with early symptomatic Alzheimer’s disease were treated with the anti-amyloid monoclonal antibodies lecanemab or donanemab and underwent amyloid PET at baseline and 6 months. Amyloid clearance measured by global Centiloids and regional SUV ratios was heterogeneous across brain regions, with regional patterns varying by clinical diagnosis and stage. These results suggest that treatment target engagement and response assessment may require regional PET metrics rather than relying solely on global amyloid measures.

Ghirelli A, Cecchetti G, Spinelli EG et al. · Alzheimer’s & dementia (Amsterdam, Netherlands) · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of Evogliptin and Dapagliflozin on Bone and Glucose Metabolism in Postmenopausal Women with Type 2 Diabetes: A Multicenter Randomized Exploratory Clinical Trial.

This multicenter randomized exploratory trial enrolled postmenopausal women with type 2 diabetes to compare 48-week treatment with the DPP-4 inhibitor evogliptin versus the SGLT2 inhibitor dapagliflozin, focusing on bone and glucose metabolism outcomes. The study evaluated how each drug affected glycemic parameters alongside bone-related endpoints over the intervention period. The findings are relevant for selecting glucose-lowering therapy that balances diabetes control with fracture risk considerations in postmenopausal women.

Ryu HJ, Park SY, Kim HY et al. · Diabetes, metabolic syndrome and obesity : targets and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Isolated granulomatous pulmonary artery vasculitis associated with Hughes-Stovin syndrome: a case report.

This case report describes a 71-year-old man with Hughes-Stovin syndrome presenting with progressive dyspnea and chest pain, where serial imaging showed rapid enlargement of a main pulmonary artery aneurysm. Histopathology of the resected pulmonary artery demonstrated granulomatous arteritis, supporting an isolated granulomatous pulmonary artery vasculitis phenotype within the HSS/Behçet-spectrum framework. The report highlights diagnostic challenges and the value of surgical pathology in rare vascular vasculitides.

Healy J, Urriola N, Nicholson I et al. · European heart journal. Case reports · (2026) · View on PubMed ↗ · Free PDF ↗

Non-pharmacological executive function interventions for children and adolescents with neurodevelopmental disorders: a systematic review and network meta-analysis.

A systematic review, pairwise meta-analysis, and network meta-analysis of randomized controlled trials evaluated non-pharmacological executive function interventions for children and adolescents with neurodevelopmental disorders (NDDs). The analysis compared effectiveness across intervention types and executive-function domains for task-based outcomes. This helps clinicians and researchers prioritize which behavioral or educational strategies most effectively improve executive functioning in specific NDD subgroups.

Liang X, Chen M, Chan RCF et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Insulin signaling in PCOS/PMOS: molecular insights and clinical implications.

This narrative review synthesized molecular and clinical evidence on insulin signaling alterations in PCOS/PMOS, focusing on pathway-level changes linking metabolic dysfunction to reproductive pathology. It highlights impaired PI3K/Akt signaling affecting insulin-dependent GLUT4 glucose uptake, compensatory hyperinsulinemia from β-cell responses and reduced hepatic insulin clearance, and downstream effects that increase free androgen bioavailability and ovarian androgen production. The review clarifies mechanistic targets for therapies aimed at breaking the metabolic–reproductive cycle in PCOS/PMOS.

Goel A, Grover A, Shekhar S · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

CLDN18 and FGFR2 splicing variants are emerging tumor-associated antigens for cancer therapy.

This review summarizes evidence that alternative splicing variants of CLDN18 (claudin-18 isoform 2, CLDN18.2) and FGFR2 (FGFR2b) act as tumor-associated antigens and discusses therapeutic development targeting these isoforms. It highlights first-generation monoclonal antibodies—zolbetuximab for CLDN18.2 and bemarituzumab for FGFR2b—and describes emerging next-generation biologics. The work supports splicing-derived antigen selection as a strategy for precision cancer immunotherapy and drug development.

Katoh M, Katoh M · Frontiers in molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Melatonin supplementation in multiple sclerosis: a systematic review of clinical, imaging, biomarker, and safety outcomes.

This systematic review evaluated oral melatonin supplementation in adults with multiple sclerosis (MS), synthesizing randomized and prospective non-randomized intervention studies and assessing clinical, imaging, biomarker, and safety outcomes. Across included studies, melatonin was investigated as a modulator of immune, oxidative, and circadian pathways, but the review concluded that overall clinical benefit and safety remain insufficiently established due to heterogeneity and methodological limitations. These findings support continued, better-designed MS trials to determine whether melatonin can meaningfully improve patient outcomes and to clarify risk–benefit for routine use.

Nabil Y, Ghazou A, Abodabesh S et al. · Frontiers in neurology · (2026) · View on PubMed ↗ · Free PDF ↗

From PCOS to PMOS: reframing the clinical pathway around insulin sensitivity and weight-neutral metabolic risk.

This Perspective article reframed the clinical pathway from polycystic ovary syndrome (PCOS) to polyendocrine metabolic ovarian syndrome (PMOS) by focusing on insulin sensitivity and weight-neutral metabolic risk in people with PCOS. It argues that insulin resistance can function as an actionable management hub for reproductive endocrine dysfunction and longer-term metabolic risk in a substantial subgroup, while noting it is not universal. The proposed naming and care framework is intended to shift clinical attention beyond ovarian morphology and body size toward metabolic risk stratification and targeted interventions.

Jiao H, Guo H, Liu J · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting TREM2+ and TIMD4+ Macrophages Reprograms the Tumor Microenvironment and Enhances PD-1 Blockade Efficacy in Intrahepatic Cholangiocarcinoma.

This study investigated intrahepatic cholangiocarcinoma (ICC) tumor microenvironment macrophage heterogeneity, focusing on TREM2+ and TIMD4+ macrophages, and tested how targeting these populations affects PD-1 blockade efficacy. The key finding was that reprogramming TREM2+ and TIMD4+ macrophages remodeled the tumor microenvironment and enhanced the effectiveness of PD-1 blockade in ICC. Clinically, this suggests a macrophage-targeting strategy could improve immunotherapy responses in ICC patients by overcoming pro-tumor myeloid programs.

Li Y, Liu H, Xu L et al. · Cancer communications (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Clonal Hematopoiesis Accelerates Frailty and Functional Decline.

This analysis tested whether clonal hematopoiesis of indeterminate potential (CHIP) and autosomal mosaic chromosomal alterations are associated with incident frailty and faster functional decline in 730,088 participants from UK Biobank, All of Us, BioVU, and the Women’s Health Initiative. CHIP and autosomal mosaic chromosomal alterations showed strong associations with frailty across multiple frailty measurement approaches, while mosaic loss of chromosome X or Y did not. These results support a mechanistic link between age-related somatic mosaicism and functional decline, potentially enabling risk stratification for frailty based on blood clonal genotypes.

Zhao K, Quin C, Pershad Y et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Proteasomal surveillance of exposed cysteines.

This preprint studied how cells surveil proteins with exposed cysteine residues by systematically analyzing the stability of thousands of cysteine-containing peptides and identifying the responsible degradation pathways. It found two complementary surveillance mechanisms: an E3 ubiquitin ligase set (including AMBRA1, TRPC4AP, FBXO3, and FBXO21) that detects double cysteines and drives ubiquitin-dependent proteasomal degradation, and a second pathway mediated by the P [truncated] component. Scientifically, the work defines how proteasomal quality control prevents proteome damage from reactive cysteines, informing future studies of redox/proteostasis-linked disease mechanisms.

Mena EL, Dong KC, Kairouz A et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Case Report: Recurrence of recipient-derived erythropoiesis in hematopoietic stem cell transplant for sickle-cell anemia: multi-lineage chimerism analysis as a tool to distinguish atypical pure red cell aplasia from poor erythroid engraftment.

This case report examined hematopoietic stem cell transplant (HSCT) in a patient with sickle-cell anemia (SCA) who developed recurrence of recipient-derived erythropoiesis, using multi-lineage chimerism analysis to distinguish atypical pure red cell aplasia from poor erythroid engraftment. The key finding was that multi-lineage chimerism patterns could be used diagnostically to differentiate these clinically similar post-transplant failure scenarios. This is significant for transplant management in SCA, because it can guide interpretation of mixed chimerism—especially under reduced-intensity conditioning—and inform subsequent therapeutic decisions.

Geurten C, Willems E, Dhedin N et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

ALS/FTD-linked TDP-43 alterations prevent HSV-1 infection by disrupting cell-adhesion pathways.

This preprint studied whether ALS/FTD-linked TAR DNA-binding protein 43 (TDP-43) alterations affect viral infection, testing cell-autonomous protection against herpes simplex virus type 1 (HSV-1) across neural and non-neural cell types, patient-derived cells, and animal models. It found that ALS/FTD-associated forms of human TDP-43 prevented HSV-1 infection by disrupting cell-adhesion pathways, and this protective effect was conserved across multiple TDP-43 mutations including sporadic ALS and C9ORF72-ALS. These results are significant because they connect TDP-43 pathology to antiviral phenotypes, offering a mechanistic framework for how neurodegenerative disease states may influence susceptibility to neurotropic viruses.

Jackvony Infurna S, Ijaz L, Hardin EJ et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Functional Exhaustion Limits CAR-NK Therapy in Glioblastoma but Can Be Mitigated by Early Repeated Dosing.

This preclinical study evaluated functional exhaustion as a limitation of allogeneic CAR-NK therapy in glioblastoma and tested whether early repeated dosing could mitigate it, comparing B7H3/CD28z CAR-NK with CAR-T cells. The key finding was that CAR-NK cells became functionally exhausted in glioblastoma, but early repeated dosing reduced exhaustion and improved therapeutic performance. This is clinically relevant because dosing schedules may be a practical lever to enhance durability of CAR-NK efficacy in solid tumors like glioblastoma.

Chaudhry K, Muniraj N, Lang H et al. · Research square · (2026) · View on PubMed ↗ · Free PDF ↗

A Human Genome-wide CRISPR-Cas9 Screen Reveals Host Factors That Support Epstein-Barr Virus B cell infection.

This preprint used a human genome-wide CRISPR-Cas9 screen to identify host factors that support Epstein–Barr virus (EBV) B-cell infection, focusing on steps after entry. The key finding was the discovery of multiple new host factors and pathways beyond known EBV receptors/co-receptors (including CD21/CR2, MHC class II, and R9AP) that support post-entry infection. Scientifically, these results expand the map of EBV dependency factors and may reveal targets to prevent EBV-driven diseases such as lymphomas and EBV-associated autoimmune risk.

Wang H, Yeo YY, Wang C et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Prion-induced heritable states in Caenorhabditis elegans.

This preprint investigated whether prion-induced protein conformations can generate heritable states in the metazoan Caenorhabditis elegans, using a yeast prion domain fused to a host protein to track transmission across generations. The key finding was that the induced altered state could be inherited transgenerationally in C. elegans, indicating prion-like heritable information beyond unicellular systems. This is significant because it supports a broader biological principle for how protein conformations can encode persistent phenotypes in animals, informing models of prion diseases and age-related neurodegeneration.

Ilbay O, Zabinsky RA, Lozanoski T et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Serum IgM crosslinks hepatitis B subviral particles into supramolecular immune complexes.

This study used cryo-electron tomography to image hepatitis B surface antigen (HBsAg)-enriched serum from a patient with severe acute hepatitis B and characterized how hepatitis B virus (HBV) subviral particles (SVPs) interact with anti-HBs antibodies, focusing on IgM. The authors found that IgM crosslinked HBsAg-rich SVPs into supramolecular, three-dimensional immune complexes that persisted even at lower particle densities, supported by spatial-randomization analysis and cryo-ET/subtomogram averaging. These structural insights explain how abundant HBV SVPs can form persistent IgM immune complexes in human blood, informing understanding of HBV immunopathology and potential biomarker/therapeutic strategies targeting SVP–antibody interactions.

Liu C, Dhawan A, Yao X et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Creation of a High-Resolution, Continually Evolvable Lineage Tracer.

This preprint describes the creation of a high-resolution, continually evolvable lineage tracer to study retinal progenitor cell (RPC) contributions to multigenerational cell diversity in the retina. The key advance is a lineage-tracing system designed to improve resolution and allow iterative evolution of the tracer to better interrogate lineage rules across generations. This provides a new tool for mapping how specific RPCs generate the ~130 retinal cell types, enabling more precise mechanistic tests of biased versus other lineage models.

Delgado RN, Si Y, Andersen RE et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

CD3-engaging bispecific antibodies convert human regulatory T cells into cytotoxic effectors.

This study investigated how CD3-engaging bispecific T cell engager (BTCE) antibodies remodel human FOXP3+ regulatory T cells (Tregs) in patients with newly diagnosed multiple myeloma (NDMM) treated in a phase 2 BTCE-based induction trial (GMMG-HD10/DSMM-XX/MajesTEC-5). The authors report that CD3-engaging BTCEs convert human Tregs into an AP-1-imprinted hybrid cytotoxic state that contributes to tumor clearance, supported by longitudinal bone marrow and peripheral blood sampling. Clinically, this clarifies a mechanism by which BTCEs can repurpose Tregs to enhance anti-myeloma immunity and guides rational combination with existing treatment backbones.

Michel JJ, Frenking JH, Metzler AD et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Clonally Expanded CD8 T Cells in AML Adopt an NK-Like Program Distinct from Canonical Exhaustion.

This study profiled bone marrow CD8 T cell clonal architecture and differentiation states in 46 newly diagnosed acute myeloid leukemia (AML) patients using mass cytometry, single-cell RNA sequencing, and single-cell T cell receptor (TCR) sequencing. It found that clonally expanded AML-associated CD8 T cells adopt an NK-like program characterized by terminally differentiated effector memory re-expression of CD45RA (TEMRA) rather than canonical exhausted T cell states. Scientifically and potentially therapeutically, this defines a distinct CD8 T cell state in AML that could be targeted or leveraged to improve immunotherapies beyond exhaustion-focused strategies.

Chu YE, Cottam MA, Potts CR et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

MHC restriction is structurally encoded by the T cell receptor germline.

This work tested whether MHC restriction is encoded by the T cell receptor (TCR) germline independent of antigenic peptide by engineering “germline-like” TCRs lacking CDR3 peptide specificity and using a molecular clamping strategy to trap ultra-low-affinity peptide-MHC complexes for cryo-EM. The authors found that germline-like TCR/pMHC docking modes match wild-type TCR docking across distinct peptide antigens and MHC alleles, providing direct structural evidence for germline-encoded recognition of MHC. This advances fundamental immunology by showing that the TCR germline structurally specifies MHC recognition, shaping how adaptive specificity is built on a conserved recognition scaffold.

Wang N, Borowska MT, Jude KM et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Early life social isolation primes flies for more rapid TDP-43 dependent neurodegeneration later in life.

This study examined whether early-life social isolation primes flies for later-life neurodegeneration driven by TDP-43 by using Drosophila models with TDP-43-dependent pathology. The key finding is that social isolation during early life accelerates or worsens TDP-43-dependent neurodegeneration later in life, indicating that psychosocial stress can causally modulate neurodegenerative risk. These results support a mechanistic link between stress exposure and TDP-43 proteinopathy, providing a tractable in vivo model for identifying upstream modifiers of ALS/FTD progression.

MurthyGowda S, Huyghue K, Castillo B et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Failure to release from the ER translocon induces 60S ribosome degradation.

This study used a pulse-chase CRISPR screening strategy in mammalian cells to identify regulators of ribosome turnover and found that loss of protein UFMylation promotes degradation of the 60S ribosomal subunit. It showed that normal UFMylation releases 60S from the ER translocon, whereas without UFMylation, ER-associated 60S accumulates and is degraded via translocon-associated large subunit degradation (TLSD) that is lysosome-independent in the human cell model. Scientifically, this defines a specific ER-translocon quality-control pathway for ribosome disposal and identifies UFMylation as a key regulator of proteostasis.

Levine ZG, Khandwala S, Zhang CJ et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Plasmid architecture determines the stability of inverted terminal repeats in adeno-associated virus vectors.

This study used a mouse model of congenital infection with Oropouche virus (OROV) to determine how maternal and fetal antiviral mechanisms change across gestation. It found that dams infected during early gestation resist severe OROV disease, mid-gestation infection leads to maternal susceptibility and death, and fetal pathology is substantial after early gestation infection. These stage-dependent outcomes highlight when fetal protection fails during pregnancy, informing timing and mechanistic targets for preventing congenital viral disease.

Jaskula-Ranga V, Li S, Pandya A et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

BI-TfR1 CapX rapidly transits the blood-brain barrier for efficient, low-dose gene delivery throughout the CNS.

This preprint investigated how plasmid architecture affects inverted terminal repeat (ITR) stability in adeno-associated virus (AAV) vector plasmids used for gene therapy production. The key finding is that structural features of the plasmid determine the propensity for ITR deletions/mutations during propagation, contributing to plasmid heterogeneity. This is significant for improving AAV manufacturing reliability by guiding plasmid design choices that preserve ITR integrity and vector consistency.

Chan KY, Lin CY, Huang Q et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Fetal-intrinsic antiviral mechanisms emerge over the course of gestation.

This study evaluated BI-TfR1 CapX, a human transferrin receptor (TfR1)-binding AAV capsid, for low-dose, systemically delivered gene transfer across the CNS in adult humanized TFRC mice. The authors found that CapX rapidly transits the blood-brain barrier, binding CNS vasculature within minutes and delivering genomes to parenchymal nuclei within 24 hours, achieving >80% cortical and spinal neuron transduction and ~60% cortical astrocyte transduction after low intravenous dosing. This supports CapX as a promising BBB-crossing capsid for efficient, low-dose CNS gene delivery with reduced peripheral distribution compared with AAV9.

Philip DT, Merlino MS, Kennedy EA et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

BAP1 loss and PRAME expression converge to remodel the tumor-immune ecosystem during uveal melanoma progression.

This study profiled 190,535 cells across normal uvea, uveal nevus, and primary/metastatic uveal melanoma using single-cell transcriptomics, T cell receptor sequencing, spatial transcriptomics, and isogenic perturbation models to determine how BAP1 loss and PRAME expression remodel the tumor-immune ecosystem. The authors report that tumor progression follows a transcriptional continuum with loss of differentiation and emergence of neural crest-like, stress-responsive, hypoxic-glycolytic, and immune-interacting states, with BAP1 loss and PRAME converging on immune-ecosystem remodeling (abstract truncated before full mechanistic details). These findings link two dominant UM prognostic axes (BAP1 and PRAME) to specific immune microenvironment states, supporting more precise stratification and combination immunotherapy strategies in uveal melanoma.

Dollar JJ, Liu X, Singh M et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Topological Engineering of NIR-II Emissive Conjugated Oligomers With Unexpected Excited-State Manifolds for Efficient Phototheranostics and Cancer Immunotherapy.

This work studied topology-driven excited-state engineering of NIR-II emissive conjugated oligomers to optimize both fluorescence and phototherapeutic performance for phototheranostics and cancer immunotherapy. The key finding is that precisely manipulating molecular topology tailors excited-state manifolds and multi-channel excitation dynamics, improving light-harvesting and exciton utilization to enable synergistic excitation regulation (abstract truncated before specific in vivo/immune outcomes). Scientifically, it provides a design framework for next-generation NIR-II theranostic materials that could couple imaging with phototherapy and immune activation.

Yang Y, Gao Y, Li N et al. · Angewandte Chemie (International ed. in English) · (2026) · View on PubMed ↗ · Free PDF ↗

Not Just Th2: Eosinophil-Associated Proteomic Networks Reveal Fundamental Differences Between COPD and Asthma.

This study examined bidirectional associations between blood eosinophil counts and COPD versus asthma using Cox proportional hazards models and bidirectional two-sample Mendelian randomization in 302,370 UK Biobank participants, with additional Olink proteomics in 32,121 participants. The key finding (details truncated in the abstract) is that eosinophil-associated proteomic networks differ between COPD and asthma, indicating distinct underlying mechanisms rather than a shared eosinophil-driven pathway. Clinically, this supports more mechanism-informed targeting of eosinophils and helps explain why eosinophil-directed therapies may benefit asthma differently than COPD.

Wu X, Fan J, Ding H et al. · Allergy · (2026) · View on PubMed ↗ · Free PDF ↗

Lipoprotein(a)-dependent cardiovascular risk in different populations: are thresholds the same?

This article reviewed and analyzed lipoprotein(a) [Lp(a)]-dependent cardiovascular risk across populations, focusing on whether clinical thresholds for Lp(a) are consistent despite ancestry-related differences in baseline Lp(a) levels. The key finding is that Lp(a) concentrations vary by ancestry (with African ancestry showing the highest median levels, as stated in the abstract), implying that risk interpretation and screening thresholds may not be transferable without adjustment. This is significant for implementing Lp(a) screening and Lp(a-lowering therapies equitably and effectively across diverse populations.

Mansfield BS, Raal FJ, Kovanen PT et al. · Annals of medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Knowledge, Attitudes, and Reported Practices Regarding Prediabetes Among Hypertensive Patients With Abdominal Obesity: A Cross-Sectional Structural Equation Modeling Analysis.

This cross-sectional study assessed prediabetes knowledge, attitudes, and reported practices among 446 hypertensive adults with abdominal obesity using questionnaire data analyzed with Spearman correlations and structural equation modeling (SEM). The key finding is that the observed KAP relationships fit a hypothesized knowledge–attitude–practice structure, with the primary practice construct defined by specific items after handling near-zero loadings (full results truncated). The clinical significance is that it identifies modifiable KAP components to inform targeted education and behavior-change interventions to prevent progression from prediabetes in high-risk hypertensive patients.

Chen J, Cao X, Zhang J et al. · Journal of diabetes research · (2026) · View on PubMed ↗ · Free PDF ↗

The genetic landscape of myotonic dystrophy type 1: insights from nearly one million genomes.

This study used whole-genome sequencing (WGS) from nearly one million participants to map CTG repeat expansions in the DMPK gene underlying myotonic dystrophy type 1 (DM1), quantify ancestry-specific distribution, and relate expansions to clinical phenotypes including cardiac manifestations and early-onset cataracts. The key finding is that large-scale WGS reveals DMPK repeat expansions across diverse ancestries and provides a more accurate estimate of population burden than clinically ascertained cohorts (abstract truncated before quantitative results). Scientifically and clinically, it improves understanding of DM1 genetic epidemiology and supports earlier risk identification for cardiac and cataract complications.

Rahman RP, Futema M, Behr ER et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

From oncogenesis to approval: the lentiviral gene therapy revolution in Wiskott-Aldrich syndrome.

This review article examined the lentiviral gene therapy approach for Wiskott-Aldrich syndrome (WAS), an X-linked immunodeficiency caused by pathogenic variants in the WAS gene leading to absent/dysfunctional WASp. The key finding is that ex vivo autologous gene therapy using lentiviral vectors can restore WASp expression in corrected hematopoietic stem/progenitor cells and has progressed from early vector trials toward clinical approval pathways (abstract truncated before specific trial outcomes). The significance is that it frames lentiviral gene therapy as a transformative alternative to allogeneic stem cell transplantation, potentially reducing donor-availability and transplant-toxicity limitations.

Karimizadeh Z, Kalantari A, Behfar M et al. · Regenerative medicine · (2026) · View on PubMed ↗

Antisense Oligonucleotides that Are Toxic to Prion-Infected Mice Share an Emergent Mechanism.

This study investigated why certain gapmer antisense oligonucleotides (ASOs) delivered into cerebrospinal fluid become fatal in late-stage prion-infected mice but not in uninfected mice. The key finding is that ASO toxicity is compound- and disease-stage dependent and is associated with an emergent transcriptomic response signature appearing ~7 days post-dose, driven chiefly by decreased expression of astrocyte-expressed genes (full details truncated). This is significant for improving the safety design of ASO therapeutics for neurodegenerative diseases by identifying a disease-specific molecular toxicity mechanism.

Zhao HT, O’Moore J, Sprague DA et al. · Nucleic acid therapeutics · (2026) · View on PubMed ↗

Artificial Regulatory T Cells Orchestrate Phase-Spanning Regeneration in Refractory Tissue Injuries.

This study engineered artificial regulatory T cells (ATregs) and ATreg-derived exosome-like vesicles using an MVB-inspired multivesicular architecture to enhance vesicle protection and sustained release for treating refractory tissue injuries. The key finding (abstract truncated) is that ATregs orchestrate phase-spanning regeneration, leveraging Treg-derived exosomes’ low immunogenicity and regenerative signaling while addressing limitations of conventional exosome carriers. Clinically, it supports a non-live-cell strategy for Treg-based regenerative immunotherapy with improved delivery stability and multiphase repair control.

Li B, Li J, Zhang G et al. · Advanced materials (Deerfield Beach, Fla.) · (2026) · View on PubMed ↗

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Neurodegeneration & Neuroinflammation

The Gut-Brain Axis and Neurodegenerative Diseases: From Mechanistic Pathways to Therapeutic Interventions.

This review examined how the gut-brain axis (GBA)—bidirectional signaling between gut microbiota and the central nervous system—contributes to neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. It concludes that disease-relevant GBA alterations (microbiome changes and downstream neuroimmune/metabolic signaling) are mechanistically linked to neurodegeneration and represent actionable therapeutic targets. The scientific significance is that GBA-focused interventions could complement or enable new treatments for neurodegenerative diseases lacking disease-modifying options.

Lin W, Shu Z, Liu G et al. · Probiotics and antimicrobial proteins · (2026) · View on PubMed ↗

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Cardiometabolic Risk, Diabetes & Obesity

Disrupted daily rhythms in light exposure and wrist temperature are associated with metabolic risk markers and obesity.

This observational study in 809 healthy adults from the ONTIME-MT cohort examined whether real-life 24-hour rhythms in light exposure and wrist temperature relate to metabolic risk markers and obesity. It reports that disrupted daily rhythms in light exposure and wrist temperature were associated with worse metabolic risk profiles and higher obesity risk. The clinical significance is that circadian disruption measurable in daily life may be a modifiable contributor to metabolic disease risk.

Dozzani I, Rodríguez-Martín M, Dashti HS et al. · International journal of obesity (2005) · (2026) · View on PubMed ↗

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Bone Health, Osteoporosis & Fracture Risk

Trabecular Bone Score has Limited Ability to Discriminate Fragility Fractures in Postmenopausal Women with Osteopenia: A Danish Case-Control Study.

This Danish retrospective case-control study assessed whether trabecular bone score (TBS) can discriminate fragility fractures in postmenopausal women with osteopenia. It found that TBS had limited ability to distinguish women with osteopenia who had fragility fractures from those without fractures. The significance is that clinicians should not rely on TBS alone for fracture discrimination in osteopenic postmenopausal women, highlighting the need for better risk stratification tools.

Mäkinen VN, Lyngberg A, Sølling AS et al. · Calcified tissue international · (2026) · View on PubMed ↗

Metabolic dysfunction-associated steatotic liver disease is associated with higher bone mineral density: results from NHANES.

This cross-sectional analysis used NHANES data (U.S. adults) to test the association between metabolic dysfunction-associated steatotic liver disease (MASLD) and bone mineral density (BMD). Participants with MASLD had higher BMD than those without MASLD. The scientific significance is that MASLD may not confer the expected osteopenia/osteoporosis risk and could refine how metabolic liver disease is incorporated into bone health risk models.

Liu J, Zhan H, Yi Z et al. · Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · (2026) · View on PubMed ↗

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Cell & Molecular Mechanisms (DNA replication/genome stability, proteostasis, signaling)

Switch from canonical to recombination-dependent DNA synthesis by M-CDK phosphorylation of DNA Polα.

This yeast mechanistic study investigated how mitotic cyclin-dependent kinase (M-CDK) phosphorylation regulates DNA replication by targeting DNA polymerase α (Pol α). It shows that M-CDK phosphorylation displaces Pol α from replication forks, triggers fork collapse at mitotic entry, and activates a DNA damage response when cells enter mitosis with under-replicated DNA. The scientific significance is improved understanding of how cells balance genome stability with replication stress, informing models of replication failure and genome instability.

Barba Tena JD, Montecchi R, Lambert M et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical Practice Guidelines & Policy/Health Systems

Executive Summary of the Clinical Practice Guideline on Tinnitus Update.

This article provides an executive summary of an updated clinical practice guideline for adults (≥18 years) with persistent, bothersome tinnitus (≥6 months) and is intended for clinicians managing this population. The guideline synthesizes evidence to recommend assessment and management strategies for persistent bothersome tinnitus, emphasizing patient-centered outcomes and care pathways. Clinically, it standardizes tinnitus evaluation and treatment decisions to improve quality of life for the large adult population affected by chronic tinnitus.

Adams ME, Cramer JD, Tunkel DE et al. · Otolaryngology—head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · (2026) · View on PubMed ↗

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Cardiovascular Hemodynamics, Thrombosis & Vascular Biology

ATAD-3 couples plasma membrane injury to mitochondrial Ca2+ signaling.

The study investigated how ATAD-3 regulates mitochondrial Ca2+ uptake after plasma membrane injury in C. elegans, focusing on the mitochondrial Ca2+ uniporter pathway and compensatory mechanisms in mcu-1 mutants. Using live-cell imaging and an RNAi screen, the authors found that ATAD-3 is an essential regulator that promotes delayed mitochondrial Ca2+ influx after injury, while MICU-3 acts as a negative regulator. Scientifically, it identifies an ATAD-3-dependent coupling between plasma membrane damage and mitochondrial Ca2+ signaling, suggesting a conserved stress-response mechanism beyond the canonical MCU route.

Xu S, Peng Y, Zhou H et al. · Nature communications · (2026) · View on PubMed ↗

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Neurodevelopment & Behavioral Interventions

Zebrafish behavioral phenomics reveals functional subtypes of autism risk genes.

This study used zebrafish behavioral phenomics to map autism spectrum disorder (ASD) genetic risk to functional behavioral subtypes in vivo. Using an unsupervised deep-learning behavioral profiling platform (ZeChat), it identified functional behavioral subtypes linked to specific ASD risk genes. The significance is that gene-to-phenotype stratification in an animal model can reveal biologically distinct ASD subgroups, potentially guiding more targeted therapeutic development.

Stuntzner-Gibson K, Zhang P, He B et al. · Molecular psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on October 12, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.