PubMed Trending Research Digest — October 11, 2026

Automated digest · 95 articles · 15 research areas · October 11, 2026

Overview

Across this week’s set, a dominant theme is precision medicine built from context-specific biology—whether that context is disease location (luminal Crohn’s), immune endotypes (T2-high CRSsNP, eosinophil biology across COPD vs asthma), or patient stage/trajectory (systemic sclerosis continuum, immune aging signatures). Several studies emphasize that biomarkers and therapeutic responses are not uniform: diagnostic accuracy for TB tongue-swab qPCR depends on whether testing occurs in asymptomatic community screening versus symptomatic triage, and eosinophil-associated risk pathways differ between COPD and asthma rather than mapping neatly onto a single “Th2-like” model.

A second major thread is mechanistic targeting of disease-relevant pathways, spanning oncology and neurodegeneration. In cancer, multiple papers advance next-generation immunotherapies and rational combinations—ECM-targeted CAR T “armoring,” improved CD38 recruiter geometry, strategies to overcome CAR shedding, and metabolic/epigenetic rewiring to restore immunotherapy or kinase inhibitor sensitivity. In neurodegeneration, the focus shifts toward RNA/DNA and epigenetic control (ASO toxicity mechanisms in prion disease, NATs for neurodegeneration, TDP-43-related biomarkers, and lactate-driven histone lactylation in Parkinson’s), alongside biomarker validation in Alzheimer’s (plasma tau coupling to postmortem pathology, and sleep architecture links to early Aβ dynamics).

Finally, translational and clinical implementation appears repeatedly: feasibility trials (systemic hypothermia during thrombectomy), perioperative decision tools (earlier POD2 CRP rule for anastomotic leakage), and guideline updates (infectious encephalitis, PJI prevention) show an emphasis on making evidence actionable. Together, the digest highlights a field moving toward more tailored interventions—guided by refined biomarkers, mechanistic pathway understanding, and context-aware clinical deployment.

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Inflammatory Bowel Disease (Crohn’s) & Gut Barrier Biomarkers

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

This study analyzed bidirectional associations between blood eosinophil counts and incident chronic obstructive pulmonary disease (COPD), asthma, and asthma–COPD overlap (ACO) in 302,370 UK Biobank participants, and used two-sample Mendelian randomization plus Olink proteomics in 32,121 participants. It found eosinophil-related risk and proteomic networks differed between COPD and asthma, revealing eosinophil-associated pathways that were not simply “Th2-like” across diseases. These findings support eosinophil-targeted strategies and biomarker development that are disease-specific rather than shared across COPD and asthma.

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

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

This cross-sectional questionnaire study assessed prediabetes knowledge, attitudes, and reported practices in 446 adults with hypertension and abdominal obesity, using Spearman correlations and structural equation modeling (SEM) to test a hypothesized KAP structure. The SEM results supported a revised knowledge–attitude–practice model (with scoring adjustments and a four-item practice construct) describing how KAP components relate in this high-risk population. Clinically, the work identifies modifiable KAP targets for prediabetes prevention interventions tailored to hypertensive adults with abdominal obesity.

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

A modular framework for antibody-drug conjugate biomarkers.

This Nature Reviews Clinical Oncology article proposed a modular biomarker framework for antibody–drug conjugates (ADCs) that goes beyond target expression measured by semi-quantitative immunohistochemistry. It argues that ADC activity depends on antigen abundance and accessibility, linker chemistry, payload characteristics, and tumor microenvironment context, and therefore requires biomarkers that capture these interacting determinants. Clinically, the framework aims to improve patient selection, therapeutic sequencing, and identification of resistance mechanisms to enable more rational ADC combinations.

Liu J, Ruan DY, McNamee N et al. · Nature reviews. Clinical oncology · (2026) · View on PubMed ↗

Weight changes differentially impact MASLD incidence, progression and outcomes based on genetic and metabolic risk profiles.

Using UK Biobank data, this study assessed how body weight changes over time affect incidence, progression, and outcomes of metabolic dysfunction–associated steatotic liver disease (MASLD) across genetic and metabolic risk profiles defined by polygenic risk scores and lipid accumulation product. The key finding was that weight dynamics differentially influenced MASLD trajectories and related cardiovascular disease outcomes depending on whether risk was hepatic vs systemic and on metabolic risk status. Clinically, it supports tailored weight-management strategies for MASLD prevention and risk reduction based on individual genetic/metabolic risk.

Chen L, Chieh Kow AW, Lv G et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗ · Free PDF ↗

Using strengths-based nursing to introduce the Kerala model of palliative care to Australia-a theoretical integrative narrative review.

This theoretical integrative narrative review examined how strengths-based nursing (SBN) could be used to adapt the Kerala model of palliative care (KMPC) for rural/remote settings in Australia. The key finding was a structured conceptual framework for implementing KMPC principles using SBN to address geographic and workforce barriers. Scientifically and practically, it offers a rationale for equitable, community-driven palliative care delivery in underserved Australian regions.

Cheluvappa D, Cheluvappa R · Annals of palliative medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Stepwise engagement of cingulate ensembles underlies motivational decline in chronic pain.

This mouse study used whole-brain activity-dependent tagging, projection-specific perturbations, in vivo Ca2+ imaging, and single-unit recordings in male mice to map stage-dependent anterior cingulate cortex (ACC) circuit engagement during neuropathic chronic pain. The key finding was that ACC→basolateral amygdala (BLA) projections were preferentially engaged early and drove mechanical hypersensitivity, whereas ACC→lateral habenula (LHb) projections were engaged later and contributed to impaired effortful persistence. These circuit-level insights identify temporal targets within ACC projections for interventions aimed at preventing motivational decline in chronic pain.

Xu W, Sun JY, Chu C et al. · Neuron · (2026) · View on PubMed ↗

Plasma lipopolysaccharide-binding protein (LBP), a proxy for intestinal permeability, relates to clinicopathological and immunological disease activity in inflammatory bowel disease patients at diagnosis and during disease course.

This study measured plasma lipopolysaccharide-binding protein (LBP), an indirect biomarker of intestinal permeability, in a uniquely characterized pediatric inflammatory bowel disease cohort of newly diagnosed ulcerative colitis (UC) and Crohn’s disease (CD) patients across 1083 longitudinal plasma samples. Higher LBP levels tracked with clinicopathological and immunological disease activity at diagnosis and during follow-up, supporting LBP as a systemic proxy for intestinal barrier dysfunction. These findings suggest that LBP could be used to monitor intestinal permeability–linked disease activity in pediatric IBD and potentially guide barrier-healing–focused management.

Barendregt DMH, Tuk B, Hulleman-van Haaften DH et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗ · Free PDF ↗

ALIX-dependent small extracellular vesicles from tissue-resident mesenchymal cells regulate pancreatic β cell proliferation in obesity.

The study examined how ALIX-dependent small extracellular vesicles (sEVs) from PDGFRα+ tissue-resident mesenchymal progenitors regulate pancreatic β cell proliferation in mice, using Pα-ALIXKO mice with ALIX selectively deleted in PDGFRα+ mesenchymal cells and a high-fat diet obesity model. Pα-ALIXKO mice showed reduced weight gain and smaller subcutaneous adipocytes, and despite similar insulin sensitivity they had impaired glucose tolerance linked to reduced pancreatic β cell area and smaller islets. These findings indicate that mesenchymal ALIX-dependent sEV signaling is a mechanistic driver of β cell expansion during obesity and may represent a therapeutic target to preserve β cell mass in metabolic disease.

Uehara Y, Nagao H, Tobimatsu A et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Differential long-term efficacy of biologic and small-molecule therapies by disease location in moderate-to-severe luminal Crohn’s disease: a systematic review and network meta-analysis.

This study used a systematic review and Bayesian network meta-analysis of randomized controlled trials in adults (≥18 years) with moderate-to-severe luminal Crohn’s disease (CDAI 220–450) to compare long-term clinical remission (CDAI <150) and endoscopic response (≥50% SES-CD reduction at week 52) across Crohn’s disease locations. The key finding was that the relative long-term efficacy of biologic versus small-molecule therapies differed by disease location within luminal Crohn’s disease. Clinically, these location-specific comparative results can guide more tailored selection of therapies to maximize week-52 remission and endoscopic response in patients with moderate-to-severe luminal Crohn’s disease.

Dalsgarð SP, Pkb KKB, Seidelin JB et al. · Inflammatory bowel diseases · (2026) · View on PubMed ↗

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Respiratory Microbiome, Viral Infection & Pulmonary Immunity

Efficacy of Dupilumab for Patients with Chronic Rhinosinusitis without Nasal Polyps: a Randomized Double-Blind Placebo Controlled Phase II Study.

In a randomized, double-blind, placebo-controlled phase II trial, 33 adults with moderate-severe chronic rhinosinusitis without nasal polyps (CRSsNP) received dupilumab (IL-4/IL-13 pathway blockade) or placebo, with exploratory analyses by T2-inflammatory endotype. The study found dupilumab efficacy and safety signals in CRSsNP and suggested differential benefit in T2-high patients. These results support further development of dupilumab as a targeted biologic strategy for CRSsNP, particularly in T2-high endotypes.

Tversky J, Lane AP, Schroeder J et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

Follicle-associated epithelial tuft cells amplify type 2 mucosal immunity and IgA production.

This study investigated intestinal follicle-associated epithelium (FAE) cell populations in Peyer’s patches using Gfi1b-eGFP reporter mice and human biopsies, focusing on tuft cells as an additional FAE lineage distinct from microfold (M) cells. It found that tuft cells arise from Pou2f3+ progenitors and that their differentiation is reciprocally regulated by RANKL (for M cells) and interleukin-13 (IL-13) (for tuft cells), with tuft cells amplifying type 2 mucosal immunity and IgA production. These results identify tuft cells as a conserved regulator of mucosal antibody responses, informing how type 2 immune pathways can be leveraged to enhance IgA-mediated protection.

Barrón GM, Jayewickreme RD, Tran HH et al. · Science immunology · (2026) · View on PubMed ↗

Phage-ICE tandems facilitate bacterial adaptation and antimicrobial resistance spread.

This study characterized how phage–integrative and conjugative element (ICE) tandems form and spread antimicrobial resistance in bacteria, using experimental systems in Streptococcus. It found that phage-encoded integrases (IntIEPhage) drive stress-inducible excision and circularization, enabling ICE machinery to cotransfer the tandem, while impaired excision triggers a fail-safe dissemination route via transformation and RecA-dependent homologous recombination. These insights clarify how phage–ICE interactions accelerate bacterial adaptation and AMR spread, informing strategies to disrupt horizontal gene transfer.

Huang J, Zhao J, Zhan P et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Alphavirus Nsp3 protein hijacks receptor-mediated mitophagy via BNIP3L/NIX to dampen IFN response and promote viral replication.

This study investigated how alphavirus nonstructural protein 3 (Nsp3) manipulates receptor-mediated mitophagy through BNIP3L/NIX to suppress the interferon (IFN) response and enhance viral replication, using alphavirus infection models including getah virus (GETV). The key finding was that GETV infection damages mitochondrial function and that Nsp3 promotes BNIP3L/NIX-dependent mitophagy, which dampens innate antiviral IFN signaling to favor viral growth. Scientifically, it identifies a specific viral-host pathway (Nsp3→BNIP3L/NIX mitophagy→IFN suppression) that could be targeted to limit alphavirus replication.

Qi X, Zhao Y, Zhu Z et al. · Autophagy · (2026) · View on PubMed ↗

Diagnosis and Management of Infectious Encephalitis in Adults: Guidelines From the European Academy of Neurology and European Society of Clinical Microbiology and Infectious Diseases.

This European Academy of Neurology/European Society of Clinical Microbiology and Infectious Diseases guideline article synthesized current evidence to provide recommendations for diagnosis and management of infectious encephalitis in adults. The key outcome was an updated, evidence-based clinical framework (structured in PICO format) addressing modern diagnostic processes and treatment options since the 2010 guidelines. Clinically, it aims to standardize care and improve outcomes for adults with suspected infectious encephalitis amid evolving etiologies and diagnostic technologies.

Granerod J, Sellner J, Stahl JP et al. · European journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Lung microbiota dysbiosis exacerbates influenza virus infection.

This study examined how lung microbiota dysbiosis affects influenza A virus (IAV) infection by using mouse models spanning different disease-severity levels after IAV challenge. The key finding was that dysregulated pulmonary microbiota worsened influenza infection outcomes and altered host–microbe interactions during disease progression. Scientifically, it supports the idea that respiratory microbiome composition can modulate antiviral immunity and may represent a target for preventing or mitigating influenza severity.

Yin HC, Zhang XY, Liu S et al. · Microbiome · (2026) · View on PubMed ↗ · Free PDF ↗

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Tuberculosis Diagnostics & Screening Strategies

Tongue Swab Mycobacterium tuberculosis Quantitative Polymerase Chain Reaction for Community Screening of Asymptomatic Tuberculosis Versus Clinic-Based Triage of Symptomatic Tuberculosis.

This study compared tongue swab Mycobacterium tuberculosis quantitative PCR (qPCR) for community screening of asymptomatic tuberculosis (TB) versus clinic-based triage of symptomatic TB using adult household contacts and symptomatic presumptive TB patients from six sites in South Africa. The key finding was that diagnostic performance of tongue swab M. tuberculosis qPCR differed between asymptomatic community screening and symptomatic clinic triage, indicating that accuracy is context-dependent. Clinically, it informs how tongue-swab qPCR could be deployed for TB screening strategies beyond symptomatic triage.

Wood RC, Olson AM, Lochner KA et al. · Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · (2026) · View on PubMed ↗ · Free PDF ↗

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Chemotherapy-Induced Organ Toxicity & Mechanistic Targets

Sensitive detection of 4-hydroxy-2-nonenal-modified proteins in oxidative stress-related diseases.

This study developed and validated rabbit polyclonal antisera for sensitive detection of 4-hydroxy-2-nonenal (HNE)-modified proteins, using HNE-modified rabbit serum albumin (RSA-HNE) as immunogen, with testing across dot blot, ELISA, and Western blot. The key finding was that the antisera showed distinct recognition profiles and enabled detection of low-abundance HNE-protein adducts in complex extracts from uninfected and Plasmodium falciparum–infected human erythrocytes. This provides a practical immunochemical tool to study oxidative-stress–linked protein damage in metabolic, neurodegenerative, and infectious diseases.

Méndez-Cuadro D, Kamali AN, Ruiz C et al. · Journal of proteomics · (2026) · View on PubMed ↗ · Free PDF ↗

Alkylating Agent-Induced FANCL Impairment Damages Pulmonary Arterial, Venous, and Microvascular Endothelial Cells and Predisposes to PAH/PVOD.

This study investigated whether alkylating chemotherapy–induced FANCL impairment contributes to pulmonary vascular injury by using mitomycin C (MMC) and cisplatin (CDDP) rat models and cultured pulmonary arterial, venous, and microvascular endothelial cells. The key finding was that both MMC and CDDP caused PAH/PVOD phenotypes with endothelial DNA damage, apoptosis, and endothelial-to-mesenchymal transition, with MMC producing more severe pathology and FANCL impairment driving endothelial dysfunction. Scientifically and clinically, it links a specific molecular target (FANCL) to chemotherapy-associated pulmonary vascular toxicity, supporting mechanistic rationale for risk mitigation in patients receiving alkylating agents.

Liu S, Sun Y, Wu X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Reproductive Biology, Oocyte/Fertility Aging & Ovarian Aging

Surgical management of interstitial (cornual) pregnancy: a systematic review of perioperative and reproductive outcomes with meta-analysis of hospital stay.

This systematic review and meta-analysis assessed perioperative outcomes and subsequent reproductive outcomes after surgical management of interstitial (cornual) pregnancy. The key finding is a pooled characterization of surgical perioperative metrics (including hospital stay) and reproductive outcomes, including uterine rupture risk, based on extractable data from eligible reports. The clinical significance is that it synthesizes evidence to better inform counseling and surgical decision-making for a rare but high-risk ectopic pregnancy.

Marchand G, Anderson D, Mera S et al. · European journal of obstetrics, gynecology, and reproductive biology · (2026) · View on PubMed ↗

Decoding the immune regulation of ovarian aging: mechanisms and therapeutic strategies.

This review article synthesizes evidence on how age-related immune changes—immunosenescence and inflammaging—regulate ovarian homeostasis and contribute to physiological ovarian aging and pathological accelerated aging such as premature ovarian insufficiency (POI). It highlights bidirectional crosstalk between systemic immune pathways and the ovarian immune microenvironment as a mechanistic driver of ovarian dysfunction and a rationale for immune-targeted therapies. Clinically, the work frames immune modulation as a potential strategy to prevent or treat POI and other ovarian aging–associated disorders.

Wang C, Li N, Chen ZJ et al. · Human reproduction update · (2026) · View on PubMed ↗

Age-Related Lamin B1 Deficiency Activates SLC7A11-Dependent Disulfidptosis to Impair Osteogenesis via Intercepting Mitochondrial Fission.

This study examined how age-related lamin B1 (LMNB1) deficiency in senile osteoporosis (SOP) affects osteogenesis in bone marrow-derived mesenchymal stem cells (MSCs). It showed that LMNB1 deficiency causes lamina-associated domain (LAD) detachment and super-enhancer formation that upregulates SLC7A11, which then triggers SLC7A11-dependent disulfidptosis and impairs osteogenic function via mitochondrial fission-intercepted cytoskeletal disruption. The findings are clinically relevant because they define a mechanistic LMNB1→SLC7A11→disulfidptosis pathway that could be targeted to restore osteogenesis in aging-related osteoporosis.

Yu W, Li Q, Zhang W et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Vitamin D: Physiology, Pharmacology and Clinical Evidence for Supplementation-A Narrative Review.

This narrative review summarizes vitamin D physiology, pharmacology, and clinical evidence for supplementation, including sources, metabolism, pharmacokinetics, and safety. It concludes that vitamin D (often combined with calcium) consistently helps prevent and treat deficiency-related skeletal disorders in high-risk populations, while also discussing distinct roles of vitamin D, calcidiol, calcitriol, and analogues. The review is significant for clinicians because it consolidates evidence to support appropriate supplementation strategies and risk–benefit considerations.

Virtanen JK · Basic & clinical pharmacology & toxicology · (2026) · View on PubMed ↗ · Free PDF ↗

Heterogeneity in secondary follicle development buffers the lifespan of activated oocytes to optimize female fertility in mice.

This study used a Zp3-based lineage-tracing mouse model to label activated oocytes (Act-Oos) and reconstruct their developmental trajectories and folliculogenesis across the lifespan, focusing on how activated oocyte heterogeneity affects female fertility. The key finding was that Act-Oo longevity is age-dependent and is buffered by secondary follicle (SF) progression, allowing some oocytes activated early to persist into late or terminal reproductive stages to optimize long-term fertility. Scientifically, it identifies SF development as a mechanism that stabilizes reproductive output over time, informing models of how fertility is maintained with aging.

Liang J, Yang X, Li Q et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

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Stroke (Endovascular Care, Neuroprotection & Recovery Targets)

TERT is a therapeutic target for tertiary stroke prevention.

This work investigated telomerase reverse transcriptase (TERT) as a therapeutic target for tertiary stroke prevention by examining TERT’s in vivo role in neural repair and functional recovery after ischemic stroke. Using single-nucleus RNA sequencing (snRNA-seq) and related in vivo approaches, the authors identified TERT-associated mechanisms in post-stroke neural recovery. Scientifically, it positions TERT as a candidate target to develop interventions aimed at improving long-term outcomes after stroke.

Luo S, Gu T, Liang M et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

Adjuvant Systemic Hypothermia During Mechanical Thrombectomy (ReCCLAIM II): A Multicenter, Randomized, Controlled Trial.

This phase II multicenter randomized feasibility-controlled trial studied whether adjuvant systemic hypothermia could be induced during mechanical thrombectomy in patients with proximal middle cerebral artery or internal carotid artery large-vessel occlusion stroke (Alberta Stroke Program Early CT Score 6–10, onset within 24 hours). The key finding was that systemic hypothermia during thrombectomy was feasible to implement in this clinical setting (ReCCLAIM II). This supports further development of hypothermia as an adjunct strategy to reduce ischemic injury during endovascular stroke care.

Kass-Hout T, Horn C, Sun CJ et al. · Stroke · (2026) · View on PubMed ↗

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Cardiotoxicity, Cancer Therapy Toxicity & Predictive Models

Palmitic acid promotes hypertrophic memory in cardiomyocytes via KDM5A/H3K4me3.

This study combined human epidemiology and mechanistic experiments to test how palmitic acid (PA) promotes hypertrophic “memory” in cardiomyocytes via KDM5A and H3K4me3, using a UK Biobank analysis of 232,592 participants plus mouse dietary models and a transverse aortic constriction pressure-overload model. It found PA enrichment associated with heart failure risk and mechanistically implicated KDM5A-mediated H3K4me3 changes in cardiomyocyte hypertrophic memory. These results suggest epigenetic targeting of the KDM5A/H3K4me3 axis as a potential therapeutic strategy to prevent or reverse PA-driven maladaptive cardiac remodeling.

Yang K, Gao R, Shi J et al. · European heart journal · (2026) · View on PubMed ↗

Roxadustat Treatment After PCI Among Patients With ST-Segment Elevation Myocardial Infarction: A Randomized Clinical Trial.

The study conducted the ROXAMI phase 2 randomized clinical trial to test whether oral roxadustat, a HIF-prolyl hydroxylase inhibitor, reduces infarct size when administered after reperfusion in adults with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. The trial evaluated infarct size as the primary outcome with follow-up through 1 year, aiming to determine whether HIF stabilization attenuates reperfusion injury in humans. If effective, roxadustat could provide a clinically practical pharmacologic approach to limit myocardial damage after PCI in STEMI patients.

Quan W, Wang Y, Zhang M et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Cell Village Captures Populational Heterogeneity of Sunitinib Cardiotoxicity.

This study used the Cell Village platform with human iPSC-derived cardiomyocytes from 20 healthy donors to investigate interindividual variability in sunitinib-induced cardiotoxicity. The key finding was that cardiotoxic responses to sunitinib show population-level heterogeneity that can be captured by donor-derived cardiomyocyte programs. This provides a scientific basis for identifying actionable predictors of TKI cardiotoxic risk and for stratifying patients receiving sunitinib.

Kojic A, Liu Y, Belbachir N et al. · Circulation research · (2026) · View on PubMed ↗

GLP-1 receptor agonists and serious adverse events: Evidence, uncertainty and clinical implications.

This narrative review appraised evidence on serious adverse events associated with GLP-1 receptor agonists, including thyroid cancer, non-arteritic anterior ischemic optic neuropathy (NAION), suicidal behaviors/self-harm, diabetic retinopathy complications, acute pancreatitis, gallbladder/biliary disease, and intestinal obstruction. The key conclusion was that while randomized trials and mechanistic studies provide some reassurance, uncertainty remains for several rare but serious outcomes due to limitations in spontaneous reports and observational data. Clinically, it highlights which risks require monitoring and clearer patient selection while guiding clinicians on balancing GLP-1 benefits against potential harms.

Ueda P · Journal of internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗

C. butyricum Combined With Resmetirom Provides Therapeutic Benefits in MASH Associated With Gut-Liver-Brain Axis Modulation.

This study tested whether the probiotic Clostridium butyricum, alone or combined with the thyroid hormone receptor-β agonist resmetirom, improves metabolic dysfunction-associated steatohepatitis (MASH) in a high-fat-diet mouse model and modulates the gut–liver–brain axis. The combination produced greater therapeutic benefit than either treatment alone, including improved MASH outcomes and attenuation of nausea/vomiting-like responses alongside gut–liver–brain axis molecular and microbiome changes assessed by 16S rRNA sequencing. These findings support a potential adjunct strategy to enhance resmetirom efficacy and tolerability in MASH by targeting gut–liver–brain signaling.

Zhang K, Zeng Y, Wu J et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗

Mitochondrial dynamics and repair differences in two mouse models of Friedreich’s ataxia.

This study compared mitochondrial content, mitochondrial dynamics, and mitophagy in two mouse models of Friedreich’s ataxia (FA), a disease caused by reduced frataxin (FXN) expression, to understand why cardiac phenotypes diverge. The authors report model-specific differences in mitochondrial behavior that may underlie progression toward distinct FA cardiomyopathy presentations, including HFpEF-like diastolic dysfunction and HFrEF-like systolic failure. Scientifically, the results link FXN deficiency to differential mitochondrial repair/dynamics, informing mechanistic targets for FA-associated cardiomyopathy.

Salinas L, Figueroa F, Montgomery-Bowie CB et al. · The Journal of physiology · (2026) · View on PubMed ↗ · Free PDF ↗

Hip Fracture Risk of Lemborexant and Suvorexant in Comparison With Z-Drugs: A Target Trial Emulation.

This target trial emulation study used Japanese healthcare databases to compare hip fracture risk in older adults (≥65 years) newly initiating lemborexant or suvorexant versus Z-drugs. It evaluated whether the dual orexin receptor antagonists (DORAs) are associated with lower hip fracture risk than Z-drugs using cohort-based comparative methods. Clinically, the findings aim to guide insomnia medication selection in older patients by clarifying fracture risk differences among DORAs and Z-drugs.

Matsuo Y, Yamana H, Sasabuchi Y et al. · Journal of the American Geriatrics Society · (2026) · View on PubMed ↗ · Free PDF ↗

Vitamin D Deficiency, Supplementation, and Aging-Related Morbidity and Mortality Across Two Longitudinal Population Cohorts.

This longitudinal EHR study analyzed associations between vitamin D status (severe deficiency <10 ng/mL vs sufficiency >30 ng/mL) and aging-related morbidity and mortality across two large population cohorts: Leumit Health Services (LHS, Israel) and TriNetX (US). Using matched longitudinal analyses of >1.67 million serum 25-hydroxyvitamin D [25(OH)D] measurements from >468,500 adults in LHS (2009–2020) and external validation in 223,175 participants, it characterized how vitamin D deficiency tracks with long-term health outcomes. The results are significant for defining whether vitamin D deficiency is a modifiable marker or contributor to systemic aging trajectories and mortality risk.

Israel A, Weizman A, Israel S et al. · Aging cell · (2026) · View on PubMed ↗

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Heart Failure Management, Diuretics & GDMT Optimization

GDMT is Associated with Reduced Loop Diuretic Requirements, Whereas Diuretic Dose Does Not Modify GDMT Benefit in Heart Failure: STRONG-HF.

This post-hoc analysis of the STRONG-HF randomized trial (n=1,075 with post-randomization loop diuretic data) examined whether guideline-directed medical therapy (GDMT) up-titration reduces loop diuretic (furosemide-equivalent) requirements and whether diuretic dose modifies GDMT benefit in heart failure. The key finding was that higher loop diuretic dose reflected more severe heart failure, while achieving 100% of target GDMT doses was associated with reduced loop diuretic requirements and diuretic dose did not modify the benefit of high-intensity care. Clinically, this suggests that optimizing GDMT can lessen congestion medication needs without undermining the outcome benefits of intensive GDMT.

Biegus J, Davison B, Cotter G et al. · European journal of heart failure · (2026) · View on PubMed ↗

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Trauma Surgery & Resource-Dependent Vascular Injury Outcomes

Improvements in Return to Work Following Lumbar Discectomy With a Bone-Anchored Annular Closure Device.

This prospective, multicenter, single-arm post-market study evaluated whether a bone-anchored annular closure device improves return to work after lumbar discectomy in 55 high-risk patients with large annular defects. The study tested the device’s effect on functional recovery timing, using return to work as a key outcome measure. Clinically, if effective, the device could reduce reherniation-related delays and improve workforce reintegration for patients at elevated risk of reoperation.

Nunley PD, Brandon Strenge K, Huntsman K et al. · International journal of spine surgery · (2026) · View on PubMed ↗ · Free PDF ↗

New guidelines for the prevention of periprosthetic joint infection : a ten-year update.

This ten-year guideline update studied current evidence and perioperative practices for preventing periprosthetic joint infection (PJI) after arthroplasty, synthesizing updated recommendations for clinicians. The key finding is that several preventive strategies have been refined since earlier major guidelines, but high-quality evidence remains limited in many areas. Scientifically and clinically, it provides an updated framework to standardize PJI prevention while highlighting where further research is needed.

Ferrini A, He M, Papalia R et al. · The bone & joint journal · (2026) · View on PubMed ↗

Revision of Unicompartmental Knee Arthroplasty to Total Knee Arthroplasty Using the CORITM Imageless System: A Step-By-Step Surgical Technique.

This article studied a step-by-step surgical technique for revising failed medial unicompartmental knee arthroplasty (UKA) to total knee arthroplasty (TKA) using the CORI™ imageless robotic system. The key finding is the described workflow using intraoperative surface mapping and dynamic kinematic assessment to improve accuracy in bone resection and ligament balancing during conversion surgery. Scientifically and clinically, it provides a practical method to address altered anatomy and asymmetric bone loss in UKA-to-TKA revisions, potentially improving surgical precision in early aseptic loosening cases.

Croitor D, Pailhé R, Le Guen A et al. · SICOT-J · (2026) · View on PubMed ↗ · Free PDF ↗

Global Disparity Within the Management of Traumatic Abdominal Vascular Injuries: Analysis of a Global Dataset.

This secondary analysis of the Global Outcomes After Laparotomy for Trauma (GOAL-Trauma) dataset studied global patterns of traumatic abdominal vascular injuries and outcomes across resource settings and patient/system factors. The key finding was that there is substantial global disparity in the management of abdominal vascular injuries, with differences linked to both system-level and patient-level characteristics. This highlights the need to strengthen access to specialist vascular care within trauma systems to improve limb and survival outcomes.

Amoako J, Bath MF, Kohler K et al. · World journal of surgery · (2026) · View on PubMed ↗ · Free PDF ↗

Development and validation of a nomogram for predicting the probability of arthroplasty in patients with osteonecrosis of the femoral head after fibular strut grafting.

This retrospective study analyzed patients with osteonecrosis of the femoral head (ONFH) who underwent fibular strut grafting (FSG) to identify predictors of failure and to develop a nomogram predicting mid-to-long-term survival without conversion to total hip arthroplasty (THA). Using univariable and multivariable Cox regression plus Kaplan–Meier survival analysis on institutional data from February 2009 to December 2018, the authors built and validated a risk prediction tool for FSG failure. The nomogram can support individualized counseling and surgical decision-making by estimating the probability of THA after FSG in ONFH patients.

Zhang H, Luo Z, Zhu J et al. · Annals of medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Postoperative Day 2 C-reactive Protein Identifies Patients at Low Risk of Anastomotic Leakage After Colon Cancer Resection.

This multicenter diagnostic accuracy study evaluated whether postoperative day 2 (POD2) C-reactive protein (CRP) <100 mg/L can exclude anastomotic leakage (AL) after colon cancer resection in patients undergoing elective surgery with primary anastomosis. It compared POD2 CRP thresholds with the commonly used POD3 criterion and assessed POD3 CRP dynamics in patients with POD2 CRP ≥100 mg/L. Clinically, an earlier CRP-based rule could improve enhanced recovery after surgery (ERAS) workflows by safely identifying low-risk patients before POD3.

Sinimäki S, Andersen CL, Nors J et al. · Annals of surgery · (2026) · View on PubMed ↗ · Free PDF ↗

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Helicobacter pylori Epidemiology & Oral Reservoirs

Site-stratified global oral Helicobacter pylori prevalence: an updated meta-analysis of dental plaque and saliva studies (1989-2026).

This updated meta-analysis pooled site-stratified oral Helicobacter pylori prevalence from dental plaque and saliva studies (1989–2026) across 49 unique cohorts (6,247 participants, 24 countries). The key finding was that oral H. pylori prevalence varies by sampling site, and the updated evidence base incorporates newer 2024–2026 studies to refine these estimates. This improves epidemiologic understanding of the oral cavity as an extra-gastric reservoir and can inform future screening and eradication strategies.

Liu Y, Zeng Y, Hu J et al. · Journal of oral microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

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Immunology of Fibrosis (IL-13, Skin Fibrosis) & Antifibrotic Targets

IL-13 and skin fibrosis in inflammatory skin diseases.

This review article examined the role of interleukin-13 (IL-13) in skin fibrosis across inflammatory skin diseases. The key finding was that IL-13 can drive fibrotic remodeling by linking type 2 immune activation to sustained extracellular matrix remodeling and persistent immune activity, extending beyond the traditional TGF-β-centered view. Scientifically, it positions IL-13 as a mechanistic bridge between chronic inflammation and fibrosis and supports IL-13–targeted approaches as potential antifibrotic strategies.

Ikegawa N, Nguyen TM, Saito-Sasaki N et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

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Pain & Rehabilitation (Chronic Pain, Neuropathic Pain, Exercise/VR)

Ex vivo machine perfusion enables robust and widespread lipophilic-conjugated siRNA delivery to the porcine lung.

This porcine translational study tested whether normothermic ex vivo lung perfusion (EVLP) can deliver fully chemically modified docosanoic acid (DCA)-conjugated small interfering RNA (siRNA) broadly in donor lungs. In paired lungs perfused for 6–8 hours, DCA-conjugated siRNA targeting Janus kinase 1 (JAK1) achieved robust, widespread delivery ex vivo. This provides a platform for sequence-specific gene silencing in donor lungs prior to transplantation.

Buchwald JE, Tocheny CE, Kharroubi H et al. · The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanisms underlying exercise-induced pain modulation in people with multiple sclerosis - a scoping review.

This scoping review examined mechanisms of central neuropathic pain (CNP) in people with multiple sclerosis (pwMS) and summarized how exercise modulates pain, aiming to identify mechanistic approaches for treatment. The key finding is that multiple neurophysiological pathways—linked to MS-related neuroinflammation, demyelination, and sensory processing—are implicated in exercise-induced pain modulation. The clinical significance is that it consolidates mechanistic targets to guide future exercise-based interventions and improve underdiagnosed/undertreated CNP in MS.

von Glasenapp B, Jungersen RC, Szikszay TM et al. · Multiple sclerosis and related disorders · (2026) · View on PubMed ↗

Lifestyle interventions for cardiometabolic health in women with polycystic ovary syndrome: a systematic review and network meta-analysis.

This systematic review and network meta-analysis evaluated exercise and dietary lifestyle interventions for cardiometabolic outcomes in women with polycystic ovary syndrome (PCOS), comparing multiple intervention types and exploring dose-response relationships (e.g., exercise dose). The analysis identified which lifestyle strategies most consistently improved cardiometabolic domains such as anthropometry/body composition and metabolic measures. Scientifically and clinically, it supports selecting more effective lifestyle regimens for reducing long-term type 2 diabetes and cardiovascular risk in PCOS.

Zhang X, Liang Z, Sabag A et al. · Human reproduction update · (2026) · View on PubMed ↗ · Free PDF ↗

Endoscopic Spine Surgery: Evidence Maturity and the Path Forward in the United States.

This evidence-focused article reviewed the maturity of clinical evidence for endoscopic spine surgery (ESS) in the United States, comparing outcomes to microscopic and tubular techniques for lumbar disc herniation and spinal stenosis and assessing the evidence base for cervical/thoracic ESS. It concluded that lumbar ESS has comparable outcomes supported by higher-level evidence, while cervical/thoracic ESS remains limited by fewer contemporary multicenter randomized trials and reliance on retrospective single-center data. The review highlights practical barriers to adoption—learning curve, training pathways, and reimbursement—along with facility-dependent economics, guiding future trial design and implementation planning.

Kim MT, Lee S, Goh GS et al. · The Journal of bone and joint surgery. American volume · (2026) · View on PubMed ↗

Effects of probiotics on joint homeostasis and osteoarthritis: Development of microbe-gut-cartilage axis-on-a-chip.

The study developed a microbe-gut-cartilage axis-on-a-chip (MGCAoC) to test how probiotic metabolites affect human cartilage organoids under physiologically relevant oxygen gradients and fluid shear, using multiomics profiling of probiotic metabolite exposure. The chip enabled perfusion of probiotic metabolites to cartilage organoids without cross-contamination between gut and cartilage modules, and multiomics suggested probiotic metabolite-driven changes consistent with altered joint homeostasis relevant to osteoarthritis. This provides a human-relevant experimental platform to dissect microbe–gut–cartilage mechanisms and to evaluate probiotic strategies for osteoarthritis.

Liu J, Zhang N, Lei Y et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

The Feasibility of Using Virtual Reality With Debriefing as a Treatment Modality for Chronic Pain.

This mixed-methods feasibility randomized study evaluated whether fully immersive virtual reality with debriefing (IVRSOT) delivered via occupational therapy is feasible and acceptable for chronic pain management compared with standard OT (SOT). The key finding was that integrating FIVR plus debriefing into outpatient OT was feasible and acceptable, with the study designed to assess effects on pain, fear of movement, and confidence. Clinically, it supports further development of IVR-based OT interventions as a potential adjunct for chronic pain rehabilitation.

Baker NA, Baird J, Kenney M et al. · The American journal of occupational therapy : official publication of the American Occupational Therapy Association · (2026) · View on PubMed ↗

Lumbar Disc Changes on Magnetic Resonance Imaging in Asymptomatic Elite Male Soccer Players.

This retrospective observational cohort study examined lumbar disc changes on MRI in asymptomatic elite male soccer players at team entry and assessed whether disc herniation burden relates to missed training. The key finding (as framed by the hypothesis) is that asymptomatic lumbar disc herniation may be common in this population and that herniation burden may not necessarily correlate with lumbar-related missed training sessions. Clinically, it informs how frequently MRI abnormalities occur in athletes and cautions against assuming that imaging findings alone predict functional training impact.

Korkmaz T, Ince Y, Kapur K et al. · Sports health · (2026) · View on PubMed ↗

Drug treatments for fibromyalgia: systematic review and network meta-analysis of randomised trials.

This systematic review and network meta-analysis of randomized trials compared drug treatments for fibromyalgia in adults (≥18 years) using evidence searched through 13 January 2025. The key finding was a comparative effectiveness ranking across multiple pharmacologic options for fibromyalgia symptom management based on trial data. This helps clinicians and guideline developers prioritize treatments by relative benefit and informs future head-to-head research.

Zeraatkar D, Lima JP, Kirsh S et al. · BMJ medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Scoping review: biomarkers in chronic inducible urticaria.

This scoping review mapped evidence on biomarkers in chronic inducible urticaria (CIndU), focusing on diagnostic, prognostic, predictive, and treatment-response biomarkers, particularly for H1-antihistamine and omalizumab therapy. The key finding was that biomarker research is heterogeneous and uneven across these domains, with ongoing gaps in validation for clinically actionable use. This identifies priority areas for future studies to enable endotyping and personalized management of CIndU.

van den Berge FR, Simons JVL, Röckmann H et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of psychedelic drug use on neurocognitive function and the psychological and social domains of quality of life: an international online study.

This international online study (N=759) examined acute, subacute, and long-term effects of serotonergic psychedelic drug use on neurocognitive performance and quality of life in participants who completed working memory, selective attention, and visual/spatial perception tasks plus mental health and QoL questionnaires. The study found measurable associations between psychedelic use and changes in cognitive task performance and psychological/social quality-of-life domains across time horizons (acute/subacute/long-term). These findings support further controlled research on how psychedelic exposure may influence cognition and real-world functioning, informing potential psychedelic-assisted therapy risk–benefit considerations.

Stadler F, Saelens J, Henter ID et al. · Frontiers in psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodegeneration & RNA/DNA-Based Therapeutics (NATs, ASOs, Epigenetics)

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

This in vivo study tested gapmer antisense oligonucleotides (ASOs) delivered into the cerebrospinal fluid in late-stage prion-infected mice versus uninfected controls, focusing on toxicity mechanisms. Toxicity was compound- and disease-stage dependent and associated with an emergent transcriptomic signature driven largely by decreased expression of astrocyte-expressed genes over ~7 days post-dose, which was absent in uninfected mice receiving the same ASOs. Scientifically, it defines a reproducible molecular mechanism of ASO toxicity in prion disease that can inform safer ASO design and preclinical risk assessment.

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) with an MVB-like multivesicular architecture to deliver Treg-derived exosome-like regenerative signals for refractory tissue injuries, aiming to replace live Treg therapy. The ATregs orchestrated phase-spanning regeneration by combining vesicle protection with sustained release from an engineered storage microenvironment. This provides a translational platform for cell-free, regulatory-T-cell-inspired therapies that may overcome ethical and regulatory barriers of live Treg administration.

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

Multiomics landscape of systemic sclerosis: from autoantibody-positivity to established disease.

This study used integrated multiomics profiling of peripheral blood mononuclear cell transcriptomics and plasma proteomics to characterize molecular alterations across the systemic sclerosis (SSc) continuum in healthy controls, SSc-specific autoantibody-positive (SSAP) individuals, very early diagnosis of SSc (VEDOSS), and limited and diffuse SSc patients. The authors report distinct, stage-associated expression and functional enrichment patterns that track progression from the asymptomatic SSAP phase through established disease. These findings support multiomics-defined biomarkers for earlier detection and mechanistic stratification of SSc before clinical onset.

Wu F, Zhao Z, Lin W et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

Anti-HDGFL2 cryptic protein antibodies provide a sensitive readout of TDP-43 pathology and clinical disease features.

This study generated and evaluated anti-HDGFL2 cryptic exon (HDGFL2-CE) antibodies as a readout of TDP-43 dysfunction in models and tissues relevant to FTLD-TDP and motor neuron disease, including ALS. The key finding is that anti-HDGFL2-CE antibodies sensitively detect HDGFL2-CE protein expression and track with TDP-43 pathology and associated clinical disease features. This is clinically important because it provides a potentially more sensitive biomarker for TDP-43 pathology than existing measures.

Citrano KJ, Maheswari Jawahar VB, Reeves MM et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Mapping transcriptional responses to cellular perturbations with RNA fingerprinting.

This paper introduced RNA fingerprinting, a statistical framework that maps single-cell transcriptional responses from new perturbation experiments onto reference single-cell perturbation dictionaries. The key finding is that RNA fingerprinting can probabilistically assign query cells to one or more candidate genetic or chemical perturbations with accurate single-cell resolution, scaling to genome-wide screens and resolving combinatorial perturbations. This is significant because it enables causal interpretation of observational single-cell data by leveraging learned perturbation “fingerprints.”

Grabski IN, Lee J, Blair JD et al. · Cell · (2026) · View on PubMed ↗

EARLY-ALS: a multicentre study on prodromal amyotrophic lateral sclerosis.

This multicentre case-control study (EARLY-ALS) surveyed 475 ALS patients and 285 controls across 20 centers in Germany and Switzerland to characterize prodromal (pre-diagnosis) symptoms and health-related factors. It found that ALS patients reported a higher burden of prodromal complaints (OR 7.50, 95% CI 4.27–13.17; P<0.001), with increased neuro-motor, sensory, and pain-related symptoms. The significance is that it helps define an early disease window for identifying candidates for intervention trials in ALS.

Cordts I, Galhoz A, Tzeplaeff L et al. · EBioMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

The IKK complex and TBK1/IKKε are recruited to STING through distinct mechanisms to activate NF-κB signaling.

This mechanistic study examined how the STING pathway activates NF-κB signaling by determining recruitment of the IKK complex and TBK1/IKKε to STING through distinct molecular mechanisms. It found that STING engages NF-κB signaling via separate recruitment routes for the IKK complex versus TBK1/IKKε, clarifying how STING can drive both interferon and inflammatory outputs. The work provides actionable mechanistic targets for developing anti-inflammatory therapies that modulate STING-driven NF-κB activation.

Christensen AH, Jurkiewicz AJ, Jensen CS et al. · Science immunology · (2026) · View on PubMed ↗

A neuronal GPCR modifies neuropeptide signaling to suppress proteostasis in distal tissues.

This study explored how a neuronal G protein–coupled receptor (GPCR) modulates neuropeptide signaling to suppress proteostasis in distal tissues, building on prior findings involving the neuronal GPCR gene gtr-1 in the context of Aβ toxicity. It identified a neuronal GPCR–dependent signaling mechanism that alters intertissue communication to reduce proteostasis capacity in distal tissues. These findings advance understanding of how neuronal signaling can regulate organism-wide protein homeostasis and influence neurodegeneration-relevant phenotypes.

Hirbawi J, Zaretsky A, Zhu H et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Chromatin interaction landscape of epimorphic regeneration in teleost fish.

The study investigated chromatin architecture changes during regeneration in zebrafish fin regeneration, using micro-C to map chromatin loops, topologically associating domains (TADs), and A/B compartments during the transition from homeostasis to blastema formation. After amputation, alterations in chromatin looping dominated over changes in TADs and compartments, and injury-altered loop interactions were linked to genes associated with regeneration. This work clarifies how 3D genome reorganization—particularly loop remodeling—supports regenerative gene programs, informing regenerative biology and potential epigenetic intervention strategies.

Jia X, Zhang X, Lin W et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Reaction-based cryo-EM resolves the continuous conformational spectrum of CTP synthase catalysis.

The study developed a reaction-based cryo-EM approach to capture Drosophila melanogaster cytidine triphosphate synthase (CTPS) during active catalysis using natural substrates and allosteric effectors, combined with three-dimensional variability analysis. This method resolved a continuous conformational spectrum across CTPS catalysis and visualized chemical progression of 4-phosphoryl-uridine triphosphate (4Pi-UTP) formation, including a previously unobserved co-occupancy pattern of adenosine triphosphate binding. The work advances structural enzymology by enabling near-native, turnover-state visualization of dynamic catalytic intermediates, which can guide mechanism-based drug design.

Guo CJ, Wu YF, Guo SY et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

A second-generation “hypoxia in a pill” rescues neurodegenerative phenotypes across distinct mouse models.

The study tested a second-generation “hypoxia in a pill” regimen in multiple mouse models of neurodegeneration, building on prior use of the hemoglobin affinity enhancer GBT440 and the HIF-2α inhibitor PT2399 to modulate oxygen delivery and prevent compensatory erythropoiesis. The optimized small-molecule regimen rescued neurodegenerative phenotypes across distinct mouse models more effectively than the earlier formulation and addressed limitations of chronic 11% FIO2 gas delivery. These findings support oral HIF-pathway modulation as a potentially safer, scalable strategy for treating neurodegenerative diseases where chronic hypoxia has shown benefit.

Wang H, Marutani E, Zazzeron L et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

SETDB1 preferentially silences evolutionarily young retroelements.

The study examined how SETDB1 silences transposable elements (TEs), focusing on whether it preferentially targets evolutionarily young retroelements, using long-read RNA sequencing mapped to a telomere-to-telomere mouse genome assembly for single-locus resolution. Knockdown of SETDB1 or core HUSH complex factors caused robust derepression, and SETDB1 showed preferential silencing of evolutionarily young TE subsets at specific loci. This refines the mechanistic understanding of SETDB1/HUSH-mediated heterochromatin and highlights locus- and age-specific TE repression relevant to genome stability and epigenetic regulation.

Cenik BK, Wang S, Iwanaszko M et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Multiple motor proteins regulate TDP-43 anterograde axonal transport.

This study investigated how TAR DNA-binding protein 43 (TDP-43) is localized and transported in axons of H9-derived human neurons, focusing on the roles of multiple motor proteins in an ALS-relevant context. The key finding was that TDP-43 anterograde axonal transport is regulated by more than one motor protein, indicating coordinated control of TDP-43 trafficking rather than a single transport mechanism. Scientifically, this clarifies a previously underexplored axonal function of TDP-43 that may contribute to ALS-associated axonal degeneration.

Feole M, Devoto VMP, Dragišić N et al. · Acta neuropathologica · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Neuronal IL-18 Signaling in the Medial Habenula Contributes to Schizophrenia-Like Behavioral Deficits via ERK-Associated BDNF Suppression.

This work tested whether pathologically elevated neuronal interleukin-18 (IL-18) in the medial habenula (MHb) drives schizophrenia-like behaviors in an MK-801-treated rat model via ERK-associated suppression of brain-derived neurotrophic factor (BDNF). Using a multimodal approach including single-cell RNA sequencing to define the IL-18-producing cell type, it found that IL-18 signaling in MHb neurons reduces ERK-linked BDNF expression and contributes to schizophrenia-like cognitive/behavioral deficits. The findings suggest a cell-type-specific IL-18→ERK→BDNF pathway as a potential mechanistic target beyond dopamine-focused antipsychotic effects.

Sun D, Zhang C, Hou M et al. · Molecular neurobiology · (2026) · View on PubMed ↗

Nucleic acid therapeutics in neurodegenerative disorders: emerging technologies and clinical landscape.

This narrative/clinical landscape review summarized emerging nucleic acid therapeutics (NATs) for neurodegenerative disorders, including approaches such as RNA sequence targeting to reduce pathogenic gene expression and splice modulation. The key finding was that NATs are increasingly positioned as precision modalities that can directly modulate disease-relevant RNA/protein networks across conditions like ALS and Alzheimer’s disease. This supports ongoing translation of RNA-based strategies into clinical development for neurodegeneration.

Ohara M, Ishigaki S, Watts JK et al. · Molecular neurodegeneration advances · (2026) · View on PubMed ↗ · Free PDF ↗

PKD2 structural destabilization drives primary cilia degeneration and ADPKD pathogenicity.

This preprint investigated how the autosomal dominant polycystic kidney disease (ADPKD)–associated PKD2 missense variant D511V affects renal polycystin function in primary cilia using cryo-electron microscopy, primary cilia electrophysiology, and super-resolution analysis. The D511V mutation neutralized PKD2 channel voltage-sensor function and drove primary cilia degeneration, demonstrating pathogenic potential for ADPKD. Mechanistically linking a specific PKD2 variant to ciliary dysfunction advances precision understanding of ADPKD and could guide future variant-targeted therapeutic strategies.

Outeda P, Wang Q, Vien T et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Genome-wide mapping of helicase-generated ssDNA reveals Hrq1 activity at RNA polymerase III-transcribed genes.

This study developed a genome-wide sequencing strategy to map helicase-generated single-stranded DNA (ssDNA) by coupling the helicase to activation-induced cytidine deaminase (AID), producing strand-specific mutational footprints detectable by whole-genome sequencing. Using the Saccharomyces cerevisiae RecQ4-family helicase Hrq1 (a functional homolog of human RECQL4), the authors mapped Hrq1 activity at RNA polymerase III-transcribed genes. The approach provides a near-nucleotide-resolution way to define in vivo helicase action sites, improving mechanistic understanding of RECQL4/HRQ1 genome maintenance pathways.

Regmi S, Alsulaiti N, Darling D et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Bacteria-Derived 1-Allylpiperazine Alleviates Symptoms of Parkinson’s Disease Model by Promoting Autophagy.

This study screened for neuroprotective probiotic candidates in transgenic Caenorhabditis elegans models of α-synuclein (α-syn)-induced Parkinson’s disease (PD) and identified an Escherichia coli strain (E8) that suppresses dendritic degeneration and motor deficits. The protective effect was linked to reduced α-syn aggregation and mechanistically to enhanced autophagy, with metabolomic profiling implicating bacterial metabolite activity (including 1-allylpiperazine). These findings support a gut-microbe-derived autophagy-promoting strategy as a potential therapeutic avenue for PD.

Qu M, Zhang X, Chen X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

H4K12 Lactylation Impairs Dopaminergic Neuron Energy Metabolism via the HIF-1α/NDUFS1 Pathway in Parkinson’s Disease.

This study investigated whether histone lactylation at H4K12 contributes to dopaminergic neuron energy metabolism defects in Parkinson’s disease via the HIF-1α/NDUFS1 pathway. It found elevated plasma lactate and increased global histone lactylation in 83 PD patients versus 83 healthy controls, and identified H4K12 as a key lactylation site driving metabolic impairment through HIF-1α/NDUFS1 signaling. The work is significant because it connects lactate-driven epigenetic modification to mitochondrial respiratory dysfunction, suggesting H4K12 lactylation or the HIF-1α/NDUFS1 axis as potential targets.

Liu Y, Li X, He W et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Alzheimer’s Disease Biomarkers, Sleep, and Microglial Metabolism

Tau phosphorylation from neuronal adaptation to Alzheimer’s disease.

This review synthesized evidence from human, rodent, and fly brains and neuronal cell models to examine how phosphorylated Tau (pTau) patterns relate to neuronal adaptation across physiological states and acute stress, and to Alzheimer’s disease pathology. It reports that pTau changes are consistently linked to altered Tau localization and functions affecting synaptic transmission, mitochondrial activity, RNA metabolism, and genomic integrity. The work is significant because it reframes pTau as potentially part of adaptive stress responses, informing how to interpret pTau biomarkers and mechanisms in Alzheimer’s disease.

Trouvé R, Verstreken P, Hoekstra MMB · Neuron · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell analyses of global cohorts outline determinants of immune aging and link the ratio of GZMK+ to GZMB+ Tem cells to health trajectories.

This study integrated seven large public single-cell PBMC datasets plus a new cohort of 2,609 ostensibly healthy individuals to map determinants of immune aging and relate immune signatures to health trajectories, focusing on CD8+ T-cell effector memory subsets. It found that the ratio of GZMK+ to GZMB+ Tem cells distinguishes healthy from pathology-associated aging trajectories and helps explain heterogeneity in immune aging. The scientific significance is that a specific CD8+ T-cell ratio could serve as a quantitative immune-aging biomarker linked to future health outcomes.

Terekhova M, Kleverov M, Francis T et al. · Immunity · (2026) · View on PubMed ↗ · Free PDF ↗

Associations between plasma biomarker levels and quantitative postmortem neuropathologic measures in Alzheimer’s disease and related dementias.

This study assessed whether plasma Alzheimer’s disease blood-based biomarkers (p-tau217, p-tau181, total tau, neurofilament light chain [NfL], and GFAP measured on the Meso Scale Discovery platform) correlate with quantitative postmortem neuropathology in 124 participants from the MADRC Longitudinal Cohort Study. The key finding was that specific plasma biomarker levels showed quantitative associations with postmortem measures of amyloid-beta (Aβ) plaques and tau-related pathology (including AT pathology), supporting blood–brain pathology coupling. These results strengthen the scientific validity of plasma biomarkers for reflecting underlying neuropathology and can improve interpretation of biomarker-based clinical trials and diagnosis.

Bianco CR, Rabaneda-Lombarte N, Fatima H et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Plasma eMTBR-tau243 as a disease biomarker across Alzheimer’s disease clinical phenotypes.

This study evaluated plasma eMTBR-tau243 and p-tau217 across Alzheimer’s disease clinical phenotypes by measuring plasma biomarkers in 20 Aβ-PET–positive AD patients representing four phenotypes and 10 cognitively unimpaired controls. The key finding was that eMTBR-tau243 (and p-tau217) varied in relation to tau pathology as reflected by tau and Aβ-PET, supporting eMTBR-tau243 as a disease biomarker across phenotypic presentations. This helps refine biomarker selection for stratifying AD patients and monitoring tangle pathology beyond amyloid status.

Whitwell JL, Bhaskaran JG, Satoh R et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Spatiotemporal heterogeneity and dynamic evolution of microglial glucose metabolic reprogramming in Alzheimer’s disease.

This review synthesized evidence on spatiotemporal heterogeneity in microglial glucose metabolic reprogramming across Alzheimer’s disease stages, brain regions, and plaque-associated microenvironments. The authors proposed a dynamic state–composition model in which multiple microglial metabolic states coexist and their proportions/spatial distribution shift as AD progresses. Scientifically, this framework links metabolic phenotypes (e.g., glycolysis and oxidative phosphorylation) to neuroinflammation and impaired clearance, guiding future mechanistic and therapeutic targeting of microglial metabolism.

Chen Y, Li F, Zhang J et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Longitudinal associations of rapid eye movement (REM) sleep and slow-wave sleep with plasma Alzheimer’s disease biomarkers.

This longitudinal cohort study followed 64 cognitively unimpaired older adults who underwent polysomnography near baseline and provided plasma twice over 2.6 years, measuring plasma Aβ42 and Aβ40 by mass spectrometry. The key findings were that frontal slow-wave activity (SWA) was inversely associated with cross-sectional plasma Aβ42/40, and low REM sleep percentage predicted a larger longitudinal decline in annualized blood-based Aβ42/40. These results suggest sleep architecture—particularly REM and slow-wave activity—may track early Alzheimer’s disease biomarker progression and could inform prevention strategies.

Hwang J, Figueredo LF, Valencia DI et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Therapeutics & Translational Oncology (including ADCs, CAR/NK, PROTAC, PI3K, immunotherapy)

Protective effects of icariin in atherosclerotic cardiovascular disease: mechanistic basis, post-ischemic protection and translational limitations.

This review synthesized experimental and translational evidence on icariin (ICA), a prenylated flavonol glycoside from Epimedii Folium, across atherosclerotic plaque biology and ischemic injury models. It concluded that ICA shows mechanistic benefits in post-myocardial infarction remodeling and ischemia–reperfusion injury (including cerebral ischemia), while also highlighting limitations in pharmacokinetics, metabolism, toxicology, and formulation/quality control that constrain translation. The review frames where ICA has strongest preclinical support and what data gaps must be addressed for clinical development in atherosclerotic cardiovascular disease.

Wang X, Yu Z, Li X et al. · Pharmaceutical biology · (2026) · View on PubMed ↗ · Free PDF ↗

Human-specific morphoregulatory signatures in basal radial glia characterise neocortex evolution.

This study compared chromatin and transcriptional profiles of neural progenitor cells isolated from gorilla, chimpanzee, and human cerebral organoids to identify human-specific cis-regulatory changes in basal radial glia. It discovered morphoregulatory regulatory signatures that gained activity in humans, characterizing cis-regulatory elements linked to neocortex evolution. Scientifically, it provides a genomic regulatory explanation for how basal radial glia programs may have been remodeled during human neocortical expansion.

Schütze TM, Kolodziejczyk A, Ditzer N et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

The conformation-selective PI3Kδ inhibitor roginolisib in patients with advanced or metastatic cancer, including metastatic uveal melanoma: first-in-human clinical trial.

This first-in-human clinical trial evaluated roginolisib, a selective non-ATP competitive PI3Kδ inhibitor that locks PI3Kδ into an inactive allosteric state, in patients with advanced or metastatic solid and hematologic cancers including metastatic uveal melanoma (mUM). In dose-escalation and expansion cohorts (24 patients in Part A; 20 mostly pretreated mUM patients in Part B), the study primarily assessed safety and explored dosing achieving continuous PI3Kδ inhibition in mUM. The results support roginolisib’s clinical feasibility as a PI3Kδ-targeted therapy and inform further development of PI3Kδ inhibition strategies in mUM and other malignancies.

Di Giacomo AM, Simonelli M, Losurdo A et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

The landscape of hepatocellular carcinoma recurrence after liver transplantation: a nationwide 14-year study.

This nationwide retrospective study analyzed recurrence of hepatocellular carcinoma (r-HCC) after liver transplantation in 388 patients across 15 French transplant centers from 2008–2020, including assessment of temporal trends and the impact of AFP model implementation in 2013. The key finding was the characterization of r-HCC recurrence patterns and post-recurrence survival/overall transplant outcomes over time, showing how evolving selection criteria and management strategies influenced prognosis. Clinically, the results provide contemporary evidence to refine post-transplant risk stratification and surveillance strategies for r-HCC.

Ningarhari M, Leray M, Coilly A et al. · JHEP reports : innovation in hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Switching from mepolizumab to benralizumab in eosinophilic granulomatosis with polyangiitis (EGPA).

This retrospective study evaluated switching therapy from mepolizumab to benralizumab in eosinophilic granulomatosis with polyangiitis (EGPA) patients who failed mepolizumab. The key finding was that benralizumab was effective and had an acceptable safety profile after mepolizumab failure, consistent with its enhanced eosinophil depletion. This supports benralizumab as a practical next-line biologic option for refractory EGPA patients.

Cottu A, Mattioli I, Groh M et al. · Chest · (2026) · View on PubMed ↗

Berberine increases the sensitivity of sorafenib in human hepatocellular carcinoma via inducing HIF-1α-mediated energy crisis.

This preclinical study tested whether berberine (BBR) can overcome resistance to sorafenib (SORA) in human hepatocellular carcinoma (HCC) by inducing a HIF-1α-mediated energy crisis, using in vitro and in vivo models plus transcriptomic/metabolomic analyses and genetic rescue experiments. The key finding is that BBR increases SORA sensitivity by activating HIF-1α-dependent metabolic stress that disrupts cellular energy homeostasis in SORA-resistant HCC. This is significant because it suggests a metabolic combination strategy (BBR + SORA) to improve outcomes in advanced HCC with drug resistance.

Guo W, Feng Z, Hu M et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Modulating pMMR colorectal tumors toward a dMMR-like phenotype by Xian-Lian-Jie-Du decoction enhances anti-PD-1 efficacy.

This study evaluated whether the Chinese medicinal decoction Xian-Lian-Jie-Du (XLJDD) can reprogram proficient mismatch repair (pMMR) colorectal tumors toward a deficient mismatch repair (dMMR)-like phenotype to enhance response to anti–PD-1 therapy. Using isogenic pMMR/dMMR mouse models and mechanistic dissection with bioactive compound screening, it found that XLJDD enhances anti–PD-1 efficacy by promoting dMMR-like features in pMMR tumors. The significance is that it proposes a potential adjunct therapy to expand immunotherapy benefit beyond the small fraction of naturally dMMR CRC patients.

Li Y, Xu L, Zhang C et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Phase I/II Study of Bavdegalutamide, a Proteolysis-Targeting Chimera Androgen Receptor Degrader, in Metastatic Castration-Resistant Prostate Cancer.

This phase I/II clinical trial evaluated bavdegalutamide (ARV-110), a proteolysis-targeting chimera (PROTAC) androgen receptor (AR) degrader, in adult males with metastatic castration-resistant prostate cancer (mCRPC) previously treated with an AR pathway inhibitor. The key finding (from the trial’s reported aims and early results) is that bavdegalutamide was tested for safety and antitumor activity to establish the recommended phase II dose (RP2D) and characterize efficacy in this heavily pretreated population. The clinical significance is that it tests a next-generation AR-targeting strategy—AR degradation rather than inhibition—for mCRPC patients with limited options after AR-pathway inhibitor failure.

Gao X, Garmezy B, Vuky J et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Targeting SUV39H2 exon skipping reverses resistance to CDK4/6 inhibitors via transcriptional activation of p21.

This study investigated a splicing-driven resistance mechanism in estrogen receptor–positive breast cancer by analyzing how exon 2 inclusion in the histone methyltransferase gene SUV39H2 contributes to overexpression in CDK4/6 inhibitor–resistant cells. It found that targeting SUV39H2 exon skipping using gapmer antisense oligonucleotides or a methyltransferase inhibitor reversed CDK4/6 inhibitor resistance and activated transcription of the cell-cycle inhibitor p21. The work supports a clinically relevant therapeutic strategy to overcome CDK4/6 resistance by manipulating SUV39H2 splicing and restoring p21-mediated growth control.

Yu S, Gong X, Yang Y et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Extracellular matrix-targeted TNC-scFv armoring enhances CAR T cell persistence and antitumor activity in solid tumors.

This study engineered an extracellular matrix–targeted CAR T cell platform by secreting a tenascin-C (TNC)-specific single-chain variable fragment (TNC-scFv) linked to conventional CAR architecture to locally target TNC in solid tumors. It found that TNC-scFv–armored CAR T cells enhanced cytotoxicity, improved persistence, and reduced exhaustion in vitro and in xenograft tumor models. The results suggest that ECM-targeted “armoring” can overcome solid-tumor physical and immunosuppressive barriers to improve CAR T efficacy.

Chen K, Fu Q, Zhang W et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

A dual-functional antiviral and anticancer peptide to target intricate host-pathogen interacting proteins of human papillomavirus associated with head and neck cancer.

The study analyzed head and neck squamous cell carcinoma (HNSCC) with human papillomavirus (HPV) by retrieving HNSCC transcriptomic profiles and HPV genes involved in host–pathogen interactions, then performing host–pathogen and protein–protein interaction network analyses to identify validated viral and host hub genes. It proposed and evaluated a dual-functional peptide designed to target intricate host–pathogen interacting proteins relevant to HPV-associated head and neck cancer. The results support a host–pathogen–directed therapeutic concept that could simultaneously disrupt HPV-driven oncogenic processes and improve anticancer efficacy.

Ashok G, Ghosh S, Sengupta S et al. · PloS one · (2026) · View on PubMed ↗ · Free PDF ↗

IGF2BP1 in 17q-gain cooperates with MYCN to regulate purine biosynthesis and immunotherapy efficacy in neuroblastoma.

The study investigated how IGF2BP1, an m6A RNA reader, cooperates with MYCN in neuroblastoma with 17q gain to regulate purine biosynthesis and immunotherapy efficacy, using CRISPR-based functional screening and mechanistic assays centered on PAICS. It identified IGF2BP1 as a critical MYCN collaborator that activates PAICS, driving de novo purine biosynthesis and promoting aggressive neuroblastoma behavior. By linking metabolic rewiring to therapeutic response, the study suggests IGF2BP1–PAICS–purine pathway targeting could improve immunotherapy efficacy in high-risk neuroblastoma with 17q-gain/MYCN amplification.

Liu J, Fang Y, Fan R et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of natural killer cell depletion on innate and adaptive immune responses to COVID mRNA vaccination.

The study assessed the role of natural killer (NK) cells in innate and adaptive immune responses to SARS-CoV-2 Spike mRNA vaccination in mice, using flow cytometry to track NK recruitment and maturation and evaluating responses under NK cell depletion. mRNA vaccination increased splenic NK populations, including CD27+CD11b+ primed NK cells and CD27−CD11b+ terminally mature NK cells over days 4–7, and NK depletion was used to determine downstream effects on Spike expression, cytokines, and Spike-specific antibody and T cell responses. These results define how NK cells shape vaccine-induced immunity, informing adjuvant or immunomodulatory strategies for mRNA vaccines.

Segard A, Goguet E, Haines-Hull H et al. · Journal of immunology (Baltimore, Md. : 1950) · (2026) · View on PubMed ↗

Optimizing the Use of Anti-CD20 Agents in Multiple Sclerosis and Other Autoimmune Central Nervous System Disorders: A Narrative Review.

This narrative review examined how anti-CD20 monoclonal antibodies (used in multiple sclerosis, neuromyelitis optica spectrum disorder, MOGAD, and autoimmune encephalitis) affect efficacy and long-term safety, focusing on B-cell depletion strategies such as extended interval dosing and dose reduction. It found that while anti-CD20 therapy robustly suppresses CNS autoimmunity, cumulative exposure increases infection risk and hypogammaglobulinemia and can blunt vaccine-induced humoral responses, motivating interval/dose optimization. Clinically, the review supports tailoring anti-CD20 dosing to balance disease control with immunosuppression-related risks and vaccine responsiveness across autoimmune CNS disorders.

Ferraro D, Abbadessa G, Azzolini F et al. · Neurology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

INSR Armoring Protects CAR-NK and CAR-T Cells Against Tumor Stroma-Induced CAR Shedding by Maintaining Cholesterol Homeostasis.

This study examined how tumor stroma–derived metabolic stress affects CAR-engineered NK and T cells, focusing on CYP27A1-derived 27-hydroxycholesterol (27HC) and the resulting CAR shedding mechanism. It found that INSR “armoring” protects CAR-NK and CAR-T cells from 27HC-induced CAR loss by maintaining cholesterol homeostasis, thereby preventing membrane cholesterol depletion and downstream lipid-raft destabilization that promotes ARF6+CD81+ microvesicle–enriched CAR release. Clinically, the approach targets a major solid-tumor barrier (stroma-driven CAR shedding) to improve durability of CAR cell therapies in gastrointestinal cancers.

Yao L, Li B, Zhang L et al. · Cancer research · (2026) · View on PubMed ↗ · Free PDF ↗

Metaplasia creates a permissive niche for select Fusobacterium species in the stomach.

This study examined how metaplasia in the stomach creates a niche for specific Fusobacterium species, focusing on Fusobacterium animalis and Fusobacterium nucleatum. It found that both species can invade cultured human gastric adenocarcinoma cells, with F. animalis showing higher adherence and invasion and hypoxia increasing bacterial survival, while exogenous GalNAc inhibited adherence and invasion. Clinically, the results support a mechanistic link between gastric tissue changes (metaplasia) and colonization by cancer-associated Fusobacterium species, informing potential microbiome-targeted interventions.

Gómez-Garzón C, O’Brien VP, Chen Q et al. · mBio · (2026) · View on PubMed ↗ · Free PDF ↗

Biparatopic targeting of CD38 using CD38-specific trimeric antibody recruiters improves cytotoxicity against multiple myeloma.

This preclinical immunotherapy study engineered biparatopic CD38 targeting using CD38-specific trimeric antibody recruiters to redirect endogenous antibodies toward multiple myeloma cells. The key finding was that biparatopic/trimeric antibody recruiter design improved cytotoxicity against multiple myeloma compared with approaches with less effective targeting geometry. This provides a rationale for next-generation CD38 recruiter therapeutics that may overcome limitations such as antigen loss or altered binding seen with existing CD38 monoclonal antibodies.

Risch H, Gebhardt AJ, Hagen N et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Immune Checkpoint Inhibitor-Induced Cardiovascular Disease: The Role of Accelerated Senescence in Vascular Dysfunction.

This review examined how immune checkpoint inhibitor (ICI) therapy can drive cardiovascular disease by promoting accelerated vascular senescence and related vascular dysfunction. It highlights mechanisms including persistent reactive oxygen species (ROS) production, mitochondrial dysfunction, and senescence-associated accumulation that disrupt vascular and immune homeostasis after ICI-induced immune activation. The work is clinically significant because it frames senescence pathways as targets to mitigate long-term cardiovascular risk in patients treated with ICIs.

Casso-Chapa B, Paniagua-Bojorges A, Palaskas NL et al. · Antioxidants & redox signaling · (2026) · View on PubMed ↗

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Generated automatically on October 11, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.