PubMed Trending Research Digest — July 18, 2026

Automated digest · 97 articles · 15 research areas · July 18, 2026

Overview

Across this week’s set of studies, a dominant theme is mechanistic immunology—how immune cell states, signaling pathways, and tissue microenvironments shape disease outcomes. Multiple papers dissect immune regulation in cancer (e.g., tertiary lymphoid structure formation/persistence, stromal IL-8–driven macrophage polarization, and NET–CAF crosstalk), while others map immune–organ interactions in neuroinflammation (microglia-driven vascular pruning, dendritic cell homeostasis via IRE1, and heterogeneous microglial responses across neurodegenerative and injury models). Together, these works emphasize that immune function is highly context- and compartment-dependent, motivating more precise biomarkers and stratified immunotherapy approaches.

A second major theme is translational precision—using new technologies and better risk models to guide treatment decisions. This includes deep learning and imaging-based prediction (pancreatic progression on serial CT; gastric surgery complication/survival prediction), improved biomarker platforms (multiplex CSF assays for ALS; functional ex vivo profiling to forecast myeloma bispecific TCE responses), and next-generation molecular tools (engineered CRISPR-like nucleases; rapid chemically synthesized RNA neoantigen vaccines; advanced spatial transcriptomics/proximity sequencing). In parallel, several clinical studies and guidelines aim to standardize care and endpoints (breast cancer surveillance consensus, barrier-integrity trial recommendations in IBD, and central review considerations in metastatic breast cancer trials), reflecting a push toward more reproducible, decision-relevant evidence.

Finally, several studies connect systemic physiology and aging biology to disease risk and therapeutic targets. Examples include climate heatwaves accelerating biological aging via metabolic dysregulation, macrophage efferocytosis dysfunction driven by prostaglandin/EP2 signaling contributing to multi-organ aging phenotypes, and metabolic/mitochondrial regulators (SIRT3 in HSC aging; mitochondrial dynamics as an inflammation checkpoint; selenium/ferroptosis pathways in septic cardiomyopathy). In neurodegeneration and related genetics, shared-risk analyses across AD/PD/LBD and new gene discoveries (e.g., H6PD biallelic variants in PD) highlight converging pathways—particularly mitochondrial and immune mechanisms—that may offer cross-disease intervention opportunities.

---

Neurodegenerative disease genetics & shared risk

Brain-first and body-first subtypes of Lewy body disease.

This review analyzed the brain-first versus body-first (BvB) subtypes of Lewy body disease, proposing that Lewy pathology initiates either in peripheral/autonomic neurons (body first) or in the olfactory bulb with subsequent spread to limbic regions (brain first). It argues that exogenous triggers such as infectious agents or toxins may initiate disease outside the CNS and that the BvB framework explains heterogeneity in clinical symptoms, imaging patterns, and post-mortem pathology. The model is significant because it can guide subtype-specific biomarker development and inform targeted prevention or early intervention strategies.

Borghammer P, Van Den Berge N, Berg D et al. · Nature reviews. Neurology · (2026) · View on PubMed ↗

Biallelic hexose-6-phosphate dehydrogenase variants cause mitochondrial dysfunction underlying Parkinson’s disease.

This genetic study examined whether biallelic variants in hexose-6-phosphate dehydrogenase (H6PD), a key enzyme in the ER pentose phosphate pathway, cause mitochondrial dysfunction underlying Parkinson’s disease (PD) by sequencing 2223 PD patients and 1229 controls (whole-exome) and 4010 PD patients and 6072 controls (whole-genome). The authors identified 13 biallelic H6PD variants in eight probands (two homozygous and six compound heterozygous), spanning early- and late-onset PD, and performed functional experiments showing mitochondrial homeostasis disruption. Clinically, this implicates H6PD as a PD-causing gene in a subset of patients and supports mitochondrial dysfunction as a mechanistic driver that could inform future targeted therapies.

Zhao M, Zhao Y, Huang J et al. · Science bulletin · (2026) · View on PubMed ↗ · Free PDF ↗

A Multimodal Deep Learning Model for Preoperative Prediction of Postoperative Complications in Gastric Cancer.

This multicenter deep learning study developed and validated a multimodal model to predict preoperatively both Clavien-Dindo (CD) grade ≥II postoperative complications and long-term survival in gastric cancer patients undergoing curative gastrectomy, using 5,237 patients from 11 Chinese centers with additional prospective validation. The key finding was that the multimodal deep learning framework outperformed existing nutritional, inflammatory, and global surgical risk scores in identifying patients at higher risk of CD grade ≥II complications and worse survival. Clinically, this could improve preoperative risk stratification and guide perioperative management and adjuvant planning for gastric cancer patients.

Ding PA, Yang S, Meng LJ et al. · Annals of oncology : official journal of the European Society for Medical Oncology · (2026) · View on PubMed ↗

Disease-predominant loci across Alzheimer’s disease, Parkinson’s disease and Lewy body dementia: evidence from the UK Biobank prospective cohort, conditional GWAS and colocalization.

This study used UK Biobank (n=322,963) to quantify cross-disorder AD–PD clinical co-occurrence with bidirectional time-varying Cox models and competing-risk sensitivity analyses, then performed conditional GWAS and colocalization using European-ancestry AD, PD, and Lewy body dementia (LBD) GWAS summary statistics. It identified disease-predominant loci across AD, PD, and LBD and used methods including LDSC, GCTA-mtCOJO/GSMR, MAGMA, SMR with HEIDI filtering, and Bayesian colocalization to distinguish shared versus disorder-specific genetic signals. These findings improve interpretation of overlapping neurodegenerative GWAS signals and help prioritize loci for mechanistic follow-up across AD, PD, and LBD.

Zhang Y, Zhang Z, Qiu S et al. · Frontiers in genetics · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neurodegeneration mechanisms & cell therapy

Transplantation of human iPSC-derived microglia ameliorates neuropathology and circuit dysfunction in progranulin-deficient mice.

This study tested whether restoring progranulin specifically in microglia can rescue disease phenotypes in progranulin-deficient mice by transplanting human induced pluripotent stem cell (iPSC)-derived microglia. Microglia-targeted progranulin restoration ameliorated neuropathology and circuit dysfunction, consistent with microglia being particularly sensitive to progranulin loss and associated complement activation. The work supports microglia-focused cell therapy as a translational approach for familial frontotemporal dementia driven by progranulin haploinsufficiency.

Davtyan H, Naguib S, Voskobiynyk Y et al. · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

Integrated 5-HT2A-TrkB and G protein signaling in serotonergic psychedelic responses.

The study developed a neural stem cell-derived in vitro model (neuronal and glial lineages) to examine how serotonergic psychedelics signal through 5-HT2A and TrkB, using a panel of tryptamines, phenethylamines, and ergolines. It found that integrated 5-HT2A–TrkB and G protein signaling pathways are engaged by psychedelic compounds in this model, linking acute receptor pharmacology to downstream neuroplastic signaling programs. This mechanistic framework supports more native-like mechanistic testing of psychedelic drugs and may help explain how acute hallucinogenic-like effects can translate into longer-lasting plasticity relevant to psychiatric therapeutics.

Taddei-Tardón M, Medina-Rodríguez L, Maltman JL et al. · Molecular psychiatry · (2026) · View on PubMed ↗

A neuroprosthesis for restoring hand movement and sensation in a person with complete tetraplegia.

The study tested a double neural bypass (DNB) neuroprosthesis in a person with complete tetraplegia, combining an intracortical brain-computer interface with targeted, patterned neuromodulation of the spinal cord and cortex. It showed real-time control of the user’s own hand movement driven by movement-intention brain signals and demonstrated longer-term sensorimotor recovery that persisted even after the system was turned off. This provides clinical proof-of-concept that hybrid brain–spinal–cortical neuroprosthetic control can restore both movement and sensation after severe spinal cord injury.

Chandrasekaran S, Wandelt SK, Jangam A et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Effectiveness of transcutaneous auricular vagus nerve stimulation in alleviating postpartum blues following cesarean delivery: A randomized double-blind controlled trial.

This randomized double-blind controlled trial studied whether transcutaneous auricular vagus nerve stimulation (taVNS) alleviates postpartum blues (PPB) after cesarean delivery in postpartum participants. Among 100 women randomized to active taVNS (n=50) versus sham (n=50) over 5 days, the active group showed a significantly smaller increase in PPB severity measured by visual analogue scale scores after mood induction on postpartum day 5. The results support taVNS as a noninvasive neuromodulation approach with potential to reduce early PPB risk following cesarean delivery.

Cheng Q, Lu M, Chen Y et al. · Journal of affective disorders · (2026) · View on PubMed ↗

Therapeutic Potential of Mesenchymal Stem Cells in Multiple Sclerosis: An Updated Review.

This updated review synthesized evidence on mesenchymal stem cells (MSCs) as a therapeutic strategy for multiple sclerosis (MS), focusing on immunoregulatory and regenerative mechanisms. The key finding is that MSCs can modulate immune responses through soluble factor release and may support neuroprotection/remyelination, making them a promising adjunct approach beyond conventional immunomodulatory drugs. Scientifically, the review frames current preclinical and clinical rationale for MSC-based therapies and identifies ongoing challenges for translating them into effective MS treatments.

Yildirim I, Biray Avci C · Molecular neurobiology · (2026) · View on PubMed ↗

---

Neuroinflammation, microglia & immune–brain interactions

Withania somnifera (Ashwagandha) as an Adjunctive Treatment to Antipsychotic Medications for Patients With Schizophrenia.

This randomized, double-blind adjunctive trial studied Withania somnifera extract (WSE; Ashwagandha) in 47 patients with schizophrenia who had a recent exacerbation, assessing symptom outcomes (PANSS, CGI, PSS) and inflammatory markers over 12 weeks. WSE treatment showed improvements compared with placebo (with results truncated in the abstract) and was evaluated as potentially acting by reducing proinflammatory markers. If confirmed in full results, Ashwagandha could represent an anti-inflammatory adjunct strategy for schizophrenia symptom management and patient stratification.

Marder SR, Kelly DL, DeVera G et al. · Journal of clinical psychopharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Microglia prune developing cortical blood vessels through PD-1 signaling.

This study examined microglia-mediated vascular pruning in the frontal cortex of postnatal day 11 mice using visualization and manipulation of microglia–vessel interactions. It found that microglia progressively approach developing cerebral vessels and mediate their pruning, with the PD-L1–PD-1 signaling axis identified as a key regulatory pathway. The results link immune-cell signaling to cerebrovascular refinement, offering a mechanistic target for understanding and potentially modulating developmental vascular disorders.

Zhang M, Wang Y, Yang R et al. · Nature neuroscience · (2026) · View on PubMed ↗

Heterogenous microglial reactivity contrasts with stable vascular transcriptional programs in mouse models of Alzheimer’s, CADASIL, and Traumatic Brain Injury.

This study used single-cell transcriptomics (>250,000 cells) to compare cerebrovascular and microglial responses across mouse models of Alzheimer’s disease (AD), traumatic brain injury (TBI), and CADASIL. It identified two previously unknown vascular endothelial/vascular cell subtypes and showed that microglial reactivity is heterogeneous while vascular transcriptional programs remain relatively stable across disease stages. These findings suggest that neuroinflammation-driven microglial states may not directly dictate consistent vascular gene programs, informing how vascular-targeted therapies might be stratified by cell-type and disease context.

Bjørnholm KD, Li H, Del Gaudio F et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

The unfolded protein sensor IRE1 is essential for homeostatic dendritic cell maturation.

This work investigated how the unfolded protein response sensor IRE1 regulates homeostatic maturation of conventional type 1 dendritic cells (cDC1s) in the context of apoptotic cell engulfment. Loss of IRE1 impaired cDC1 (but not cDC2) homeostatic maturation and survival, with IRE1 activation depending on apoptotic uptake and cholesterol influx and proceeding via a steady-state IRE1-dependent decay program rather than a canonical unfolded protein response. The results position IRE1 as a key mechanistic control point for dendritic cell homeostasis and immune regulation, with potential relevance for therapies targeting UPR/IRE1 signaling.

Bosteels V, Maréchal S, Cloots E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

International consensus on intestinal epithelial barrier assessment and therapeutic effects in inflammatory bowel diseases clinical trials.

This international consensus article developed recommendations for assessing intestinal epithelial barrier integrity and for designing clinical trials targeting barrier healing in inflammatory bowel disease (IBD). It focused on how to select endpoints and evaluate therapeutic effects in trials where barrier restoration is the intended mechanism. The consensus is significant because it standardizes trial design and barrier assessment methods, which should improve comparability across studies and accelerate development of barrier-directed therapies.

Vieujean S, Atreya R, Buda A et al. · Gut · (2026) · View on PubMed ↗

Efficacy and safety of duvakitug in patients with ulcerative colitis (RELIEVE UCCD): a phase 2b, randomised, placebo-controlled trial.

This phase 2b, multicentre, randomized, placebo-controlled trial evaluated duvakitug, an anti-TNF-like cytokine 1A (TL1A) monoclonal antibody, in adults aged 18–75 years with moderately to severely active ulcerative colitis (including inadequate response/loss of response/intolerance to prior therapies). The study tested efficacy and safety of a 2250 mg subcutaneous loading dose followed by 450 mg or 900 mg every 2 weeks versus placebo. The results inform whether TL1A blockade with duvakitug provides clinically meaningful symptom control and mucosal benefit in UC patients who have failed conventional or advanced treatments.

Reinisch W, Stepek D, Kempinski R et al. · The lancet. Gastroenterology & hepatology · (2026) · 1 citations · View on PubMed ↗

Pathophysiology of irritable bowel syndrome.

This review summarized current evidence on the pathophysiology of irritable bowel syndrome (IBS), integrating peripheral mechanisms (eg, post-infectious changes, microbiome alterations, visceral hypersensitivity, increased intestinal permeability, low-grade mucosal inflammation/immune changes, motility abnormalities, and roles of serotonin, bile acids, and carbohydrate metabolism) with central mechanisms (psychological health and altered central pain processing). The key finding is that IBS likely arises from interacting peripheral and central abnormalities rather than a single defect, despite the lack of a definitive biomarker. This integrated model supports more personalized, mechanism-based approaches to IBS treatment and future biomarker discovery.

Nasser Y, Shin A, Ford AC et al. · The lancet. Gastroenterology & hepatology · (2026) · View on PubMed ↗

α6GABAA receptor-selective positive allosteric modulator as a novel therapy for fibromyalgia: A proof-of-concept study in mice modeling chronic widespread musculoskeletal pain.

This proof-of-concept study tested whether an α6GABAA receptor-selective positive allosteric modulator (PAM) can treat fibromyalgia-like pain in mice. In ICR mice modeling chronic widespread musculoskeletal pain using dual acidic-saline injections and intermittent cold stress, the pyrazoloquinolinone compound 6 and the deuterated candidate DK-I-56-1 reduced mechanical allodynia and thermal hyperalgesia. These preclinical results support α6GABAA receptor-selective PAMs as a promising therapeutic direction for central sensitization–driven fibromyalgia.

Sant-Cassia M, Lee CH, Phani Babu Tiruveedhula VVN et al. · Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · (2026) · View on PubMed ↗ · Free PDF ↗

Direct interaction of Vδ7 TCRs with IL17RA drives the differentiation of TH1-like γδT cells.

This mouse study investigated how Vδ7 γδT cell receptors (Vδ7 TCRs) recognize endogenous ligands by testing whether interleukin-17 receptor A chain (IL17RA) can act as a γδTCR ligand. IL17RA directly interacted with germline-encoded regions of the Vδ7 chain to drive differentiation of Vδ7+ γδT cells toward a TH1-like effector program with selection of a diverse CDR3 repertoire. The finding identifies IL17RA as a defined ligand for γδTCR-driven effector programming, informing how γδT cells are regulated for immune responses.

Ye K, Francis N, Dunst J et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

IL-7-glucose-Aiolos axis orchestrates pathogenic CD8+ T cell function in spondyloarthritis.

This human immunology study defined a metabolically distinct subset of CD8+ T cells in spondyloarthritis characterized by high CXCR3, IL-7R, and GLUT1 and low Aiolos expression. IL-7–JAK–STAT signaling increased GLUT1 expression and glucose uptake while reducing Aiolos, and Aiolos acted as a regulatory constraint on effector cytokine production under glucose availability. The IL-7–glucose–Aiolos axis provides a mechanistic target for controlling pathogenic CD8+ T cell function in inflammatory disease.

Akiyama M, Alshehri W, Koroyasu M et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Endosomal MrGPRX1 signaling sensitizes TRPV1 to enhance itch.

This study examined how endosomal signaling by the GPCR MrGPRX1 sensitizes the TRPV1 channel to enhance itch. Using mechanistic experiments (details truncated), the authors propose that intracellular/endo-somal MrGPRX1 signaling amplifies TRPV1 responsiveness, increasing pruriceptive signaling. The work advances a cell-compartment–specific model of itch signaling that could inform targeted therapies for chronic pruritus.

Duran P, Retamal JS, de Amorim Ferreira M et al. · Frontiers in molecular neuroscience · (2026) · View on PubMed ↗

---

Neurodevelopmental & epigenetic regulation

Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.

This study used the genetically tractable model organism C. elegans to test whether early-life modulation of the TIP60/NuA4 acetyltransferase complex can program adult proteostasis capacity and longevity. Reducing NuA4/TIP60 activity during a critical early-life window enduringly enhanced proteostasis and extended lifespan, mechanistically involving depletion of H4K16ac and compensatory early-life-biased, XBP-1-mediated unfolded protein response. The findings suggest that targeting NuA4 complex activity early in life can establish long-term resilience against proteostasis collapse relevant to aging and neurodegeneration.

Wang Y, Xiong X, Zhang R et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

Pioneer transcription factors direct tissue-specific cohesin chromatin entry and three-dimensional genome organization.

This work investigated how the cohesin loader NIPBL is recruited to tissue-specific chromatin sites, focusing on pioneer transcription factors in human genomic datasets and motif/chromatin immunoprecipitation-sequencing analyses. It identified FOXA1 as a key mediator of tissue-specific NIPBL recruitment to intratopologically associating domain (TAD) regions, while ETS factors help position NIPBL at TAD boundaries to support asymmetric versus symmetric loop extrusion. These findings clarify how pioneer factors specify 3D genome architecture and provide a mechanistic basis for tissue-selective gene regulation through cohesin dynamics.

Wang S, Zhang X, Jia T et al. · Nature genetics · (2026) · View on PubMed ↗

Missense but mis-spliced: germline TP53 variant c.671A > C (p.E224A) and the path from uncertainty to pathogenicity.

Researchers characterized the germline TP53 variant c.671A>C (p.E224A) in a 2-year-old child with retroperitoneal rhabdomyosarcoma and a family history suggestive of Li-Fraumeni syndrome, using functional assays in yeast and human cells. They found that the variant is missense but mis-spliced, producing functional impairment consistent with pathogenicity rather than benign uncertainty. This improves variant interpretation for TP53 and supports more accurate clinical risk assessment and surveillance decisions in suspected Li-Fraumeni syndrome.

Velkova I, Cappato S, Rivera D et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

The minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses in Drosophila melanogaster.

Researchers modeled minor spliceosome dysfunction by generating a CRISPR/Cas9-induced U4atac mutant in Drosophila melanogaster targeting the conserved stem II region. U4atac homozygous mutants showed growth and neurodevelopmental defects, immunodeficiency, and gastrointestinal symptoms, and the study found that the minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses. This links U4atac-dependent splicing to a conserved cytokine signaling pathway, providing mechanistic insight into how U4atac mutations could drive immune phenotypes in humans.

Shikara D, Bishop E, Barton N et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Boron-bridged GIPCs stabilize cell wall anchoring and PIN polar domains.

This study examined how boron (B) regulates plant plasma membrane organization by linking glycosylinositol phosphorylceramides (GIPCs) to PIN-FORMED (PIN) auxin transport proteins, focusing on PIN2 polar domain stability. B cross-links nearly all GIPC series to form physical PM–cell wall attachments (Hechtian strands), and B-mediated GIPC–PIN2 interactions restrict PIN2 lateral diffusion and endocytosis, stabilizing polar domain formation. The findings connect a micronutrient requirement (boron) to auxin transport polarity via direct lipid–protein stabilization of PIN domains.

He M, Zhang C, Li Z et al. · Cell · (2026) · View on PubMed ↗

A transcriptional biosensor reveals mechanisms of α-ketoglutarate signaling to chromatin.

This study used a transcriptional biosensor to investigate how the metabolite α-ketoglutarate (αKG) is regulated in the nucleus to control chromatin demethylation in human cells and in a mouse model. The key finding is that nuclear αKG is supplied by an interorganelle pathway requiring sequential mitochondrial GPT2 activity and the SLC25A11 transporter, and that GPT2 deficiency causes histone hypermethylation in the brain with dysregulated neurodevelopmental gene expression. Scientifically, it links a specific metabolic transport/signaling mechanism to epigenetic control, and clinically it provides mechanistic insight into neurodevelopmental consequences of inborn errors of metabolism affecting αKG production.

Sternisha AC, Li H, Gajendra K et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Cross-cohort analysis of expression and splicing quantitative trait loci in TOPMed.

This study analyzed expression and splicing quantitative trait loci (e/sQTLs) using 14,324 RNA-seq samples from the TOPMed program across six tissues/cell types, including whole blood and lung. The authors found tens of thousands of secondary cis-e/sQTLs and reported that secondary cis-e/sQTL discovery remains unsaturated, then fine-mapped UK Biobank GWAS signals from 164 traits and identified e/sQTL colocalizations for 10,611 GWAS signals. These results expand the catalog of regulatory variants affecting gene expression/splicing and improve mechanistic interpretation of complex-trait GWAS loci across human tissues.

Orchard P, Blackwell TW, Kachuri L et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

A cinnamyl alcohol dehydrogenase-like scaffold organizes monoterpenoid indole alkaloid biosynthesis.

This plant biochemistry study investigated how monoterpenoid indole alkaloid (MIA) biosynthesis—specifically formation of the labile strictosidine aglycone intermediate—overcomes a spatial bottleneck between strictosidine β-glucosidase (SGD) and geissoschizine synthase (GS). The authors discovered VinBLAST, a cinnamyl alcohol dehydrogenase-like scaffold that physically mediates SGD–GS interaction in the nucleus and allosterically enhances GS catalytic efficiency, improving processing of the unstable intermediate. By enabling efficient conversion toward MIAs such as vinblastine, the work provides a mechanistic scaffold strategy for engineering complex alkaloid biosynthesis.

Gao D, Mann SGA, Chen B et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Replication-uncoupled MET1/DNMT1 activity shapes inheritance of DNA methylation.

The study used live-cell CG methylation (mCG) sensors and genetic dissection in the model plant Arabidopsis to determine how replication-coupled versus replication-uncoupled maintenance of DNA methylation is regulated by MET1/DNMT1. The key finding is that mCG maintenance extends well beyond DNA replication, with the major CG methyltransferase MET1 remaining associated with chromatin from S phase through G2 phase. These results clarify how replication-uncoupled MET1 activity shapes epigenetic inheritance and suggest conserved principles for DNA methylation maintenance across eukaryotes.

Edera A, Larue M, Leduque B et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Familial pulmonary alveolar proteinosis and type I interferonopathy by mutation of STAT2 (TIMS2).

The study identified the genetic cause of familial pulmonary alveolar proteinosis with type I interferonopathy by analyzing STAT2 mutations in three siblings with early-onset, life-threatening pulmonary disease. The key finding is a novel homozygous STAT2 variant (R223Q) that preserves STAT2 signaling and viral control in vitro while disrupting feedback inhibition via USP18. This establishes STAT2 (TIMS2) as a monogenic driver of severe pulmonary IFN-I pathology and provides mechanistic insight that could guide targeted interventions.

Gruber C, Ramba M, Debnath B et al. · The Journal of experimental medicine · (2026) · View on PubMed ↗

Kinetochore clustering is mediated by Mps1 phosphorylation of conserved MELT motifs in Stu1.

This study examined how the Mps1 kinase regulates kinetochore clustering in budding yeast by phosphorylating conserved MELT motifs in the Stu1 protein and recruiting Slk19. Mps1 phosphorylates two MELT motifs in Stu1 to drive Slk19 recruitment and formation of long, string-like Stu1:Slk19 filaments that cluster unattached kinetochores. These findings define a conserved, phosphorylation-based mechanism for spindle checkpoint–linked kinetochore organization that can be targeted to modulate mitotic fidelity.

Mallett DR, Jiang M, Minnuto GM et al. · The Journal of cell biology · (2026) · View on PubMed ↗

Myelin Alteration in Neurodevelopmental Disorders: Integrating Clinical and Preclinical Evidence.

This review integrated clinical and preclinical evidence on myelin alterations in neurodevelopmental disorders (NDDs), focusing on how disrupted myelination and oligodendrocyte dysfunction contribute to disease mechanisms. It synthesizes findings across multiple NDDs, emphasizing that impaired myelin formation/maintenance during critical developmental windows increases vulnerability to genetic and environmental insults. The review highlights myelin-related pathways as potential biomarkers and therapeutic targets for NDDs.

Lubińska J, Śliwa M, Filip M et al. · Current neuropharmacology · (2026) · View on PubMed ↗

---

Cancer imaging, prediction & clinical decision support

Mitochondrial dynamics and metabolic regulation in cellular inflammation: From mechanisms to precision therapeutics.

This narrative review examined how mitochondrial dynamics—fission/fusion regulated largely by Dynamin-related protein 1 (Drp1)—link mitochondrial signaling to cellular inflammation and metabolic regulation, and how these mechanisms can be leveraged for precision therapeutics. The key finding is that pathological mitochondrial fragmentation and related mitochondrial stress promote innate immune activation via release of damage-associated molecular patterns (DAMPs) and ATP suppression, positioning mitochondrial dynamics as a therapeutic checkpoint. This mechanistic synthesis supports development of targeted interventions aimed at mitochondrial fission/fusion pathways to modulate inflammatory disease.

Park WH · Pharmacology & therapeutics · (2026) · View on PubMed ↗

Whole-transcriptome-scale isoform-resolved spatial imaging of single cells in tissues.

This study developed an in situ RNA amplification method integrated with multiplexed error-robust fluorescence in situ hybridization (MERFISH) to enable whole-transcriptome-scale, isoform-resolved spatial transcriptomics in tissues. Using the approach, the authors imaged ~33,000 distinct RNAs (including ~23,000 genes and ~10,000 isoforms) in mouse brain, enabling systematic region- and cell-type analyses at isoform resolution. The technique provides a scalable platform for mapping isoform-specific gene expression programs in intact tissues.

Cohen L, Halpern AR, Blosser TR et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial proximity sequencing maps developmental dynamics in the germinal center.

This study introduced spatial proximity sequencing (Sprox-seq) to map developmental dynamics in the germinal center by simultaneously profiling surface proteins, protein complexes, and mRNAs with tissue location. In human tonsils and germinal centers, Sprox-seq quantified 32 proteins, 528 pairwise interactions, and thousands of mRNAs, revealing higher protein-interaction complexity in the light zone and interaction trajectories that track tissue architecture. These results provide a spatially resolved framework for understanding how protein interactions drive germinal center development.

Wang H, Xia J, Rahman PMSM et al. · Cell · (2026) · View on PubMed ↗

Structure and evolution-guided design of minimal RNA-guided nucleases.

This work focused on designing minimal RNA-guided nucleases by engineering active, divergent variants of TnpB (a CRISPR-Cas12-like nuclease) using a structure-guided inverse-folding model combined with evolution-informed residue constraints. High-throughput screening of AI-generated SynTnpBs produced editors that retained or exceeded wild-type activity in bacterial, plant, and human cells, and cryo-electron microscopy provided structural validation of the designed nucleases. The approach enables creation of programmable genome-editing tools with properties not constrained by natural evolutionary limits.

Skopintsev P, Esain-Garcia I, DeTurk EC et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

De novo design of orthogonal far-red, orange, and green fluorophore-binding proteins for multiplexed imaging.

This study used de novo protein design to create orthogonal far-red, orange, and green fluorophore-binding proteins (NovoTags) that bind three cell-permeable dyes with nanomolar affinity and high selectivity. The authors tuned NovoTag fluorescent lifetimes and demonstrated multiplexed fluorescence imaging using lifetime and wavelength readouts, including a two-chain NovoTag system functioning as chemically induced dimerization with fluorescent output in living cells. These engineered binders expand the toolkit for genetically addressable, multiplexed imaging with improved dye-like photophysical performance.

Tran L, Klein S, Juergens D et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

IVT-free, chemically synthesized protein-encoding RNA oligonucleotides for rapid production of personalized cancer vaccines.

The study developed IVT-free, chemically synthesized RNA oligonucleotides designed to rapidly produce personalized cancer vaccines encoding neoantigens, using a cap-independent truncated RNA strategy. The authors report that 39-nt cap-independent chemically synthesized protein-encoding RNA oligonucleotides can be manufactured quickly without plasmid fermentation or in vitro transcription while still enabling neoantigen expression. This approach could shorten manufacturing timelines for personalized mRNA neoantigen vaccines and potentially improve treatment within the optimal therapeutic window for patients.

Pan Q, Zhang C, Wang X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Progression-Free Survival in Metastatic Breast Cancer by Local Investigators vs Blinded Independent Central Review: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis compared progression-free survival (PFS) assessed by blinded independent central review (BICR) versus local investigators in hormone receptor-positive/ERBB2-negative metastatic breast cancer trials. The key finding is that investigator-assessed PFS can differ from BICR-assessed PFS, indicating susceptibility to assessment bias even when PFS is the primary endpoint. Clinically, the results support careful consideration of central blinded review to improve endpoint validity in metastatic breast cancer trials.

Ravani LV, Bagheri Z, Kalinsky K et al. · JAMA oncology · (2026) · View on PubMed ↗

Prevention and management of anastomotic leakage after colorectal resection: evolving trends among Italian surgeons. A SICCR survey.

This SICCR survey assessed evolving real-world prevention and management practices for anastomotic leakage (AL) after colorectal resection among Italian surgeons, using a 26-item questionnaire administered to 414 respondents. The key finding is that despite multiple AL strategies being available, their application in clinical practice varies across surgeons and is influenced by experience level. The results highlight gaps between evidence-based AL management and routine practice, informing targeted education and guideline implementation efforts.

Costi R, Annicchiarico A, Amato A et al. · Updates in surgery · (2026) · View on PubMed ↗ · Free PDF ↗

Patterns of Colorectal Cancer Diagnosis in Older Adults: A SEER-Medicare Analysis of Health and Economic Impact of Missed Screening Opportunities.

This SEER-Medicare analysis studied how colorectal cancer (CRC) diagnostic pathways—screening, inpatient/outpatient (IP/OP), or emergency presentation (ER)—affect outcomes and healthcare costs in adults aged ≥65 years diagnosed between 2005 and 2019. Patients diagnosed via ER routes had worse clinical outcomes and higher healthcare utilization/costs than those diagnosed through screening or IP/OP pathways. The findings support interventions to reduce missed screening and shift CRC diagnosis away from emergency presentations to improve both survival and cost-effectiveness.

Worku EB, Woldesenbet SA, Chatzipanagiotou OP et al. · Journal of surgical oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Deep Learning Predicts Imminent Tumor Progression in Advanced Pancreatic Adenocarcinoma Using Serial CT Scans During Chemotherapy.

This study developed a spatiotemporal deep learning model combining convolutional neural networks and LSTM to predict imminent tumor progression in advanced pancreatic adenocarcinoma using serial CT scans during chemotherapy, trained on a retrospective cohort of 243 patients. The key finding was that the model could dynamically predict progression at the next follow-up visit despite RECIST 1.1 classifications of stable disease or partial response, addressing the short-term limitations of standard response assessment. Clinically, this could enable earlier identification of patients likely to progress during chemotherapy and support more timely treatment adjustments.

Cheng J, Mao Y, Huang S et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cancer immunotherapy & tumor microenvironment (TLS/TME)

Neutrophil extracellular traps induced by tumour-derived NGAL reprogram CAF subtypes via ITGA5 to promote tumour progression in pancreatic cancer.

This research investigated how tumor-derived NGAL–driven neutrophil extracellular traps (NETs) reprogram cancer-associated fibroblast (CAF) subtypes via ITGA5 to promote pancreatic ductal adenocarcinoma (PDAC) progression. It used quantitative spatial analysis of human PDAC specimens to define NET–CAF subtype interactions and to identify upstream NETosis drivers and therapeutic combination strategies targeting this axis. The study is clinically relevant because it provides a mechanistic explanation for NET-associated immunosuppression in PDAC and suggests ITGA5-centered combination approaches to overcome resistance to immune checkpoint blockade.

Liu W, Wang X, Chen R et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗

PD-1 blockade unleashes local hepatitis B virus-related B cell response inhibiting hepatocellular carcinoma.

This study examined the mechanism of perioperative anti–PD-1 therapy in patients with resectable recurrent hepatocellular carcinoma (HCC) (NCT04615143), using mechanistic analyses alongside a phase 2 trial. Single-cell multi-omics and spatially paired scRNA-seq/BCR-seq identified two tumor microenvironment subtypes—T cell–dominant versus B cell–dominant—and showed that PD-1 blockade unleashes a local hepatitis B virus (HBV)-related B cell response with somatic hypermutation that promotes antibody binding to HBcAg. The findings suggest that anti–PD-1 efficacy in a subset of HCC patients may be mediated by local B cell immunity targeting HBV antigens.

Chen S, Wang Y, Chen J et al. · Cancer cell · (2026) · View on PubMed ↗

Lymph nodes now optional.

This Science commentary discusses the emerging concept that lymph nodes may be optional for certain immune processes in cancer, in the context of how dendritic cells can orchestrate tertiary lymphoid structures within tumors. The key message is that local immune organization in tumor tissue can substitute for classical lymph node–dependent pathways in some settings. The significance is a shift in how researchers may think about designing and evaluating immunotherapies that rely on in situ immune priming rather than lymph node trafficking.

Decker WK · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Dendritic cells control tertiary lymphoid structure development and maintenance in cancer.

This study used spatial transcriptomics and multiplex imaging in human tumors and a mouse non-small cell lung cancer model to determine how tertiary lymphoid structures (TLSs) form and persist in cancer. CCR7+ mature dendritic cells (DCs) accumulated in TLSs, and early TLS development required IFN-γ-driven type 1 conventional dendritic cell (cDC1) maturation, migration to tumor-draining lymph nodes, and T cell recruitment, while later TLS persistence became independent of tdLN T cell egress and tracked with intratumoral cDC1 accumulation. These results define a DC-centered mechanism for TLS maintenance that may help predict or enhance immunotherapy responsiveness.

Mattiuz R, Boumelha J, Aerakis E et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗

Stromal-Derived IL-8 Promotes M2 Macrophage Polarization via the RhoA/MRTF-A/SRF Transcriptional Axis to Impair CD8+ T Cell Cytotoxicity in Lung Cancer.

This study investigated how stromal-derived interleukin-8 (IL-8) from DESMIN+ cancer-associated fibroblasts (CAFs) promotes M2 macrophage polarization through the RhoA/MRTF-A/SRF transcriptional axis and suppresses CD8+ T cell cytotoxicity in lung cancer. Using orthotopic and subcutaneous mouse models, Cxcr2 knockout models, and co-culture and organoid systems, the authors found that IL-8/CXCR2 signaling drives M2 polarization and impairs CD8+ T cell killing. The work identifies the IL-8→CXCR2 and RhoA/MRTF-A/SRF pathway as a mechanistic target to improve antitumor immunity in lung cancer.

Gu X, Fang Q, Yu J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell sequencing combined with transcriptome analysis unravels LUM+ B cells as key drivers in abdominal aortic aneurysm.

This study integrated single-cell RNA sequencing (scRNA-seq) with bulk transcriptome analyses from GEO datasets (GSE183464 and GSE226492) to characterize the immune microenvironment in abdominal aortic aneurysm (AAA) and identify LUM+ B cells as key drivers. It used computational approaches including cell clustering and trajectory inference (CytoTRACE2, Monocle2) to implicate LUM in B-cell-mediated AAA processes and then supported the findings with experimental validation. The work suggests that LUM+ B cells and LUM-dependent pathways may be actionable targets for modulating immune-driven vascular remodeling in AAA.

Zhang H, Peng J, Li L et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Hematologic malignancies therapeutics & trials

Asciminib monotherapy in patients with BCR::ABL1 T315I-mutated chronic-phase chronic myeloid leukemia: phase 1 trial final results.

This phase 1, nonrandomized trial reported long-term safety, tolerability, and efficacy of asciminib monotherapy in 48 patients with BCR::ABL1 T315I-mutated chronic-phase chronic myeloid leukemia (CML-CP). After a median 3.5 years of exposure, 53.3% of evaluable patients achieved major molecular response (MMR), with many maintaining or deepening responses (full details truncated). These final results reinforce asciminib’s clinical value as an ABL1 myristoyl-pocket inhibitor for a high-resistance CML-CP genotype.

Cortes JE, Rea D, Mauro MJ et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Englumafusp alfa plus glofitamab in B cell non-Hodgkin lymphoma: a phase 1 trial.

In a phase 1 open-label, nonrandomized trial, investigators evaluated englumafusp alfa (a CD19-4-1BBL co-stimulatory molecule) plus glofitamab in patients with relapsed or refractory aggressive B-cell non-Hodgkin lymphoma, with obinutuzumab pretreatment and step-up dosing of glofitamab. The study assessed safety and clinical activity across escalating doses of englumafusp alfa given alongside repeated cycles of glofitamab. If effective and tolerable, this off-the-shelf combination strategy could improve outcomes for patients with CD20-positive B-NHL who have limited options after relapse.

Hutchings M, Dickinson M, Gritti G et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

First-line ibrutinib plus venetoclax for non-blastoid mantle cell lymphoma in patients ≥65 years or with TP53 mutations.

This report analyzed the phase 3 SYMPATICO open-label cohort evaluating first-line ibrutinib plus venetoclax in older patients (≥65 years) with non-blastoid mantle cell lymphoma (MCL) or in patients with TP53 mutations (TP53m). In 78 enrolled patients, the study reported high complete response (CR) and overall response rates under a regimen of oral ibrutinib 560 mg daily plus venetoclax with a 5-week ramp-up to 400 mg daily for 2 years, followed by continued ibrutinib. Clinically, the findings support the potential effectiveness of combining BTK inhibition with BCL-2 inhibition in higher-risk MCL groups defined by age and TP53 status.

Wang M, Hoffmann MS, Wróbel T et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

---

Solid tumor targeted therapy & precision oncology

SUV39H2-mediated NCOA4 methylation controls ferritinophagy and ferroptosis in triple-negative breast cancer.

This study examined how the lysine methyltransferase SUV39H2 regulates ferritinophagy and ferroptosis in triple-negative breast cancer (TNBC) by targeting the ferritinophagic cargo receptor NCOA4. SUV39H2 directly mono-methylated NCOA4 at lysine 356 (K356), which reduced NCOA4 stability by enhancing NCOA4 interaction with the E3 ligase HERC2, promoting ubiquitination and proteasomal degradation and thereby altering FTH1 levels and ferroptosis sensitivity. These findings identify an SUV39H2–NCOA4 methylation axis as a mechanistic regulator of iron flux, with potential for ferroptosis-based therapeutic strategies in TNBC.

Liu L, Pei X, Li D et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

A DR5/Ligase 3-mediated feedback loop perpetuates immunogenicity in mismatch repair deficient colorectal cancer.

This study investigated how a DR5/Ligase 3-mediated feedback loop sustains immunogenicity in mismatch repair deficient (dMMR) colorectal cancer (CRC), using transplant syngeneic tumor models, immune cell co-culture assays, and air-liquid interface (ALI) culture of tumor-derived organoids. The authors found that DR5 and Ligase 3 signaling form a feedback mechanism that perpetuates antitumor immune recognition in MSI/dMMR CRC, helping explain why some tumors remain immunogenic while others may resist immune checkpoint inhibitor (ICI) therapy. These mechanistic insights suggest potential biomarkers and therapeutic targets to enhance or restore immunogenicity in dMMR/MSI CRC.

Hao S, Sato Y, Battaglin F et al. · Gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗

Next-generation precision oncology in microsatellite stable colorectal cancer: integrated targeting beyond RAS and RAF.

This article reviews next-generation precision oncology strategies for microsatellite-stable (MSS) colorectal cancer (CRC), focusing on integrated targeting beyond canonical RAS/RAF alterations and incorporating molecular profiling, spatial biology, and immune characterization. It highlights that MSS CRC resistance is driven by tumor heterogeneity, adaptive resistance, and an immunosuppressive tumor microenvironment (TME), motivating therapeutic approaches that extend beyond RAS/RAF pathway inhibition (including antibody-drug conjugates and other non-canonical vulnerabilities). The significance is that more comprehensive biomarker-driven and spatially informed targeting could expand effective treatment options for the large MSS CRC population that currently lacks durable precision-therapy responses.

Bartolini M, Algaze S, Lenz HJ · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

Durvalumab With Radiation Therapy in Patients With Inoperable Locally Advanced Non-Small Cell Lung Cancer Ineligible for Concurrent Chemoradiotherapy (DART).

This multicenter, single-arm prospective phase II study evaluated durvalumab given concurrently with definitive radiation therapy (RT) without chemotherapy in patients with inoperable locally advanced non-small cell lung cancer (LA-NSCLC) who were ineligible for concurrent chemoradiotherapy. The key finding is the reported efficacy and adverse-event profile of the durvalumab+RT regimen in this cCRT-ineligible population, addressing a clinical gap where standard-of-care durvalumab after cCRT does not apply. Scientifically and clinically, the results inform whether chemo-free integration of durvalumab with RT can provide a viable treatment option for frail or comorbidity-limited patients.

Rimner A, Lebow ES, Fitzgerald KJ et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Targeting WRN Helicase in Microsatellite Instable Colorectal Cancer Induces Antitumor Immunity through Extrachromosomal Circular DNA Release.

This study tested whether inhibiting the WRN helicase in microsatellite instability (MSI) colorectal cancer (CRC) cells triggers antitumor immunity via extrachromosomal circular DNA (eccDNA) release. WRN inhibition selectively induced cell death in MSI CRC cells and promoted eccDNA release that directly stimulated immune activation. These data suggest WRN helicase inhibitors could convert non–PD-1–responsive MSI CRC into an immunogenic state by engaging innate immune sensing of eccDNA.

Hao S, Sato Y, Liu Z et al. · Cancer research · (2026) · View on PubMed ↗

Simplified BALAD (BALAD-S) Score as a Guide for First-Line Immune Checkpoint Inhibitor Selection for Unresectable Hepatocellular Carcinoma.

This multicenter retrospective study evaluated whether the simplified BALAD-based score (BALAD-S), calculated from bilirubin, albumin, AFP, AFP-L3, and des-γ-carboxyprothrombin, predicts outcomes and guides first-line immune checkpoint inhibitor selection in 752 Japanese patients with unresectable hepatocellular carcinoma (uHCC). BALAD-S was associated with differential treatment outcomes between atezolizumab plus bevacizumab (Atez/Bev) and durvalumab plus tremelimumab (Dur/Tre). Clinically, BALAD-S could help personalize first-line ICI regimen choice in uHCC using routinely available biomarkers.

Hiraoka A, Tada T, Hirooka M et al. · Hepatology research : the official journal of the Japan Society of Hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cancer biomarkers & functional immune assays

Functional immune profiling translates T cell dynamics into predictive biomarkers for myeloma immunotherapy.

This study developed an image-based, high-content ex vivo functional immune profiling assay using patient-derived bone marrow mononuclear cells to predict responses to myeloma bispecific T cell engagers (TCEs) teclistamab or talquetamab. Multiplex immunofluorescence quantified plasma cell lysis, T cell expansion/morphology, and spatial engagement, revealing three functional response phenotypes (non-responder, cytotoxic, and cytotox…; truncated) across treated patient samples. The approach provides a mechanistic, single-cell biomarker framework to forecast TCE efficacy and potentially guide patient selection in multiple myeloma.

Herzberg F, Lu F, Korenkov M et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Multiomic profiling links L1 retrotransposition to genomic instability and ecDNA in bladder cancer.

This study applied integrated multi-omic profiling—including cell-free DNA sequencing, long-read tumor DNA sequencing, RNA-seq, and spatial transcriptomics—to a cohort of 48 bladder cancer patients to link LINE-1 (L1) retrotransposition with genomic instability and extrachromosomal DNA (ecDNA). It found frequent somatic L1 insertions that are active and occur early in bladder cancer development, and it connected these insertions to downstream genomic rearrangements and ecDNA formation. The work supports a causal role for early, active L1 retrotransposition in generating genomic instability, highlighting L1 activity as a potential biomarker or therapeutic target in bladder cancer.

Pribus SJ, Osredek I, Otoničar J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Multiplex Panel Detects Glial and Inflammatory Biomarker Signatures in Sporadic and C9orf72-ALS.

This study investigated whether a nucleic acid–linked immuno-sandwich assay (NULISA) multiplex platform can detect and extend CSF biomarker signatures in amyotrophic lateral sclerosis (ALS), comparing sporadic ALS with C9orf72-associated ALS. Using a targeted panel of 131 neural, glial, and inflammatory markers from minimal CSF volumes, the authors identified glial and inflammatory biomarker signatures and assessed validation/novel candidates relative to previously proposed CSF biomarkers. The significance is that NULISA could enable practical, multiplex CSF biomarker testing for ALS diagnosis/prognosis despite limited sample availability.

Baskar K, Steffke C, Bernsen S et al. · Neurology(R) neuroimmunology & neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

---

Infectious disease & host-directed therapy

The Parkinson’s disease-linked G2019S mutation of LRRK2 increases NADPH oxidase-2 activity in neutrophils for superior control of bacterial infections.

Researchers studied the Parkinson’s disease-linked LRRK2 p.G2019S mutation in mice during infection with Salmonella typhimurium or Listeria monocytogenes, focusing on neutrophil NADPH oxidase-2 signaling. They found that p.G2019S increases phosphorylation of NADPH oxidase-2 subunits p40phox and p47phox, promoting their relocation to lysosomes and enhancing bacterial control. This suggests that an LRRK2 mutation can modulate innate immune function, providing insight into shared biology between Parkinson’s disease genetics and infection susceptibility.

Hurley K, Kaul R, Yadav S et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗

Triple IFN pathway deficiency sensitizes mice to human respiratory virus infection independent of human viral receptor expression.

Researchers generated an innate-immunity severely deficient mouse model (AGL) using one-step knockouts of the interferon receptors IFNAR, IFNGR, and IFNLR to test susceptibility to human respiratory viruses independent of human viral receptor expression. AGL mice became susceptible to diverse human respiratory viruses, including adenovirus type 55 (HAdV-55), monkeypox virus (MPXV) clade IIb, and parainfluenza virus (PIV), indicating that complete IFN pathway deficiency is sufficient to permit infection. This provides a powerful preclinical model for studying human respiratory virus pathogenesis and for evaluating antiviral strategies that restore or bypass interferon signaling.

Fan Q, Pan M, Jiang M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Diversity and distinctive characteristics of the global RNA virome in urban and peri-urban environments.

This study analyzed 2,922 metatranscriptomic environmental samples from urban and peri-urban settings across 102 cities in 31 countries to characterize the global RNA virome. Using RNA-dependent RNA polymerase–based phylogenetics, it constructed the Urban & Peri-urban RNA Virus Atlas (UPVAtlas) containing 54,945 RNA viruses, 77% of which were previously unobserved, greatly expanding known evolutionary diversity. The atlas and findings are significant for understanding how environmental RNA viruses circulate in human-associated ecosystems and for improving surveillance of emerging viral threats.

Gao Z, Wu J, Lucaci AG et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Nirmatrelvir for acute COVID-19 to prevent long COVID (PANORAMIC Norway): a double-blind, randomised, placebo-controlled trial.

This double-blind, randomized, placebo-controlled trial (PANORAMIC Norway) tested whether nirmatrelvir-ritonavir given for acute SARS-CoV-2 infection reduces the risk of long COVID (post-COVID-19 condition) in non-hospitalized adults recruited from municipal health-care services in Bergen, Oslo, and Ålesund. The study compared long COVID incidence between participants receiving nirmatrelvir-ritonavir versus placebo after acute infection. If effective, this would provide prospective evidence that early antiviral treatment can prevent long COVID, informing clinical guidelines for acute COVID-19 management.

Oppegaard O, Blomberg B, Cox RJ et al. · The Lancet. Infectious diseases · (2026) · View on PubMed ↗

Gabija restricts phage circularization and DNA replication.

This study investigated how the Gabija nuclease–helicase antiphage system restricts phage circularization and DNA replication, focusing on Pseudomonas aeruginosa infected with a temperate lambda-like phage. The authors showed that phage-encoded DNA end-binding proteins that antagonize host RecBCD sensitize phages to Gabija, and that Gabija prevents phage genome circularization, blocking subsequent replication. The work clarifies a self/non-self discrimination mechanism for Gabija and advances understanding of bacterial defense against temperate phages.

Hong A, Liu M, Truta A et al. · Cell host & microbe · (2026) · View on PubMed ↗

Inflammasome activation dictates the efficacy of antimycobacterial activity of frontline TB drugs.

This study explored host-directed mechanisms underlying the enhanced antimycobacterial activity of frontline TB drugs when combined with sertraline (SRT) in murine tissues. The authors identified that SRT modulates mitochondrial physiology to generate reactive oxygen species (ROS), and they report that inflammasome activation influences the efficacy of antimycobacterial activity. These findings connect a specific host signaling pathway (inflammasome/mitochondrial ROS) to improved TB drug performance, supporting rational host-directed therapy development.

Singh A, Bisht K, Maurya G et al. · PLoS pathogens · (2026) · View on PubMed ↗ · Free PDF ↗

Oral Spermidine Supplementation Preserves Submandibular Gland Function After Radiotherapy: Mechanistic Insights and Use in a Phase II Randomized Clinical Trial.

This study tested oral spermidine supplementation in an irradiation-induced submandibular gland (SMG) injury mice model and validated mechanisms in SMG organoids, using integrated proteomic and metabolomic profiling to identify radiation-associated changes. Oral spermidine restored salivary flow, preserved acinar aquaporin-5 expression, and reduced vacuolization, apoptosis, and fibrosis after radiotherapy, with spermidine-level alterations observed during recovery. Scientifically and clinically, it supports spermidine as a mechanistically grounded radioprotector and provides rationale for a Phase II randomized clinical trial to prevent post-radiotherapy xerostomia.

Min Y, Gao K, Liu Y et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cardiometabolic disease, obesity & vascular aging

Association between the combined cholesterol, high-density lipoprotein, glucose index and frailty index and new-onset cardiovascular disease in individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: evidence from CHARLS.

This cohort analysis used CHARLS data to evaluate whether a combined cholesterol–HDL–glucose index plus a frailty index (CHG-FI) predicts new-onset cardiovascular disease (CVD), heart disease, and stroke in individuals with cardiovascular-kidney-metabolic syndrome stages 0–3. The study aimed to show that the combined CHG-FI better captures multidomain risk than single markers for middle-aged and older adults. If validated, CHG-FI could improve early risk stratification and prevention targeting before clinical CVD develops.

Sun Z, Wang K, Guo C et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Brown fat-specific RNA labelling reveals a network of inter-organ communication by secreted microRNAs.

The study used brown fat-specific RNA labeling in male mice via uracil phosphoribosyltransferase-mediated incorporation of 4-thiouracil to track extracellular microRNA (miRNA) transfer to other tissues. It found that brown adipose tissue secretes miRNAs through small extracellular vesicles and protein-associated compartments, and that these miRNAs show tissue-selective uptake in liver, muscle, and hypothalamus, with Dicer disruption in BAT depleting miRNAs in both BAT and distal tissues. This establishes a mechanistic map of inter-organ communication by secreted miRNAs and links BAT miRNA signaling to systemic energy metabolism regulation.

Lino M, Palermo-Ruiz G, Efthymiou V et al. · Nature metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Cryptogenic steatotic liver disease: a lean phenotype associated with increased liver-related mortality.

This study investigated clinical features and outcomes of cryptogenic steatotic liver disease (SLD) defined as “lean SLD” without recorded cardiometabolic risk factors (CMRFs) using UK Biobank MR-PDFF (SLD as PDFF ≥5%) and validated findings in hepatic steatosis index-based UKB and external cross-sectional cohorts including NHANES and Korean National Health Insurance Service (KNHIS). Lean cryptogenic SLD was associated with higher liver-related mortality compared with non-SLD/other groups, indicating a distinct high-risk phenotype despite absence of typical cardiometabolic risk factors. These findings suggest that “lean” patients with MRI-confirmed SLD may require liver-focused risk stratification and follow-up even when conventional metabolic risk is not documented.

Yoon EL, Lee HY, Lee J et al. · Gut · (2026) · View on PubMed ↗

FGF21 synergizes with leptin to counteract obesity-related metabolic comorbidities by reversing hepatic leptin resistance.

This study examined how fibroblast growth factor 21 (FGF21) synergizes with leptin to reverse obesity-induced peripheral leptin resistance in mice, including hepatocyte signaling via STAT1. The authors found that FGF21 acting in adipocytes increases adiponectin, which induces hepatic leptin receptor expression through STAT1 phosphorylation/activation, and that an intraperitoneal long-acting FGF21/leptin dual agonist protects mice from diet-induced weight gain more effectively than either mono-agonist. These results suggest a mechanistically grounded dual FGF21–leptin therapeutic strategy to overcome leptin resistance in obesity-related metabolic comorbidities.

Shen Q, Zou H, Jin L et al. · Cell metabolism · (2026) · View on PubMed ↗

Hypoglossal Nerve Stimulation and the Incidence of Cardiovascular Disease.

The study used a retrospective cohort design in adults with obstructive sleep apnea from the Merative MarketScan Commercial Database to test whether hypoglossal nerve stimulation (HGNS) is associated with a lower incidence of cardiovascular disease (CVD). The key finding is that HGNS recipients had a different (reported in the full text) CVD incidence compared with propensity-matched non-implanted controls meeting HGNS candidacy criteria. If confirmed, this would position HGNS not only as an OSA therapy but also as a potential strategy for cardiovascular risk reduction.

Kondamuri N, Hyman MJ, Cai Y et al. · JAMA otolaryngology— head & neck surgery · (2026) · View on PubMed ↗

Efficacy and Safety of Brensocatib in Participants of Asian Race with Non-cystic Fibrosis Bronchiectasis: A Subgroup Analysis of the ASPEN Trial.

This prespecified subgroup analysis evaluated efficacy and safety of brensocatib, a dipeptidyl peptidase 1 (DPP1) inhibitor, in Asian participants with non-cystic fibrosis bronchiectasis from the ASPEN trial. The key finding is that brensocatib reduced the annualized pulmonary exacerbation burden versus placebo over 52 weeks in this Asian subgroup while maintaining an acceptable safety profile. This supports brensocatib’s generalizability across racial subgroups and informs treatment decisions for bronchiectasis patients in Asian populations.

Addrizzo-Harris D, Chalmers JD, Aliberti S et al. · Pulmonary therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Tirzepatide and reduced risk of pulmonary embolism and deep vein thrombosis: a multicenter U.S. cohort study.

This multicenter U.S. retrospective cohort study used the TriNetX network to assess whether tirzepatide initiation in adults with type 2 diabetes and overweight/obesity is associated with reduced venous thromboembolism outcomes. After propensity score matching to patients receiving lifestyle intervention alone, tirzepatide was associated with a lower risk of pulmonary embolism and deep vein thrombosis in real-world data. These findings suggest tirzepatide may confer additional thromboembolic risk reduction beyond glycemic and weight effects, warranting confirmation in prospective studies.

Kahkedjian F, Shah J, Kreidieh F · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cardiovascular disease mechanisms & therapeutics

Mechanistic insight into signal bias by the agonist-dependent conformational dynamics of GPR84.

This study determined cryo-electron microscopy structures of the GPR84–Gi complex bound to the G protein-biased agonist DL-175 and of inactive GPR84 bound to the antagonist GLPG1205, integrating signaling assays and molecular dynamics simulations. It showed that agonist-dependent conformational dynamics create a mechanistic basis for biased agonism, including steric interactions that selectively prevent β-arrestin–related conformational changes. These insights explain how GPR84 achieves signaling selectivity and can inform the design of biased ligands to tune immune and metabolic effects.

Suzuki S, Tran DP, Nishikawa K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Human iPSC-derived engineered heart tissue model of diastolic dysfunction in heart failure with preserved ejection fraction.

This work studied whether human induced pluripotent stem cell (iPSC)-derived engineered heart tissues (hEHTs) can model heart failure with preserved ejection fraction (HFpEF)-associated diastolic dysfunction in vitro. High fatty acid plus L-NG-nitroarginine methyl ester (L-NAME) supplementation produced reduced relaxation function with preserved contraction, elevated BNP, abnormal calcium transients, and HF-like structural/functional features. The model provides a human cellular platform to dissect mechanisms and test therapies for HFpEF diastolic dysfunction.

Tani H, Haga K, Moriwaki T et al. · Cell stem cell · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists: From Clinical Success to Mechanistic Insight.

This review synthesized clinical and mechanistic evidence on glucagon-like peptide-1 receptor (GLP-1R) agonists and their cardiovascular effects in hypertension and cardiometabolic syndrome. It highlights that beyond weight loss and glycemic control, GLP-1R agonists improve endothelial dysfunction, vascular inflammation, leukocyte recruitment, atherosclerotic plaque composition, and cardiorenal pathways related to sodium regulation and neurohumoral balance. The mechanistic framing supports broader therapeutic targeting of vascular-metabolic biology to reduce cardiovascular risk.

Patel TA, Rose J, Katsurada K et al. · Circulation research · (2026) · 1 citations · View on PubMed ↗

Prevention of Vascular Aging as a Novel Paradigm for GLP-1 Receptor Agonist-Mediated Cardioprotection.

This review examined how GLP-1 receptor agonists (GLP-1RAs) may protect the cardiovascular system by preventing vascular aging. It integrates emerging evidence that GLP-1RAs improve vascular regenerative progenitor cell flux in type 2 diabetes and links these effects to multiple vascular hallmarks relevant to atherosclerosis, heart failure, peripheral artery disease, and potential chronic kidney disease benefits. The proposed vascular-aging paradigm provides a mechanistic lens for future trials and biomarker development in cardiometabolic disease.

Dennis CJ, He AZ, Krishnaraj A et al. · Circulation research · (2026) · 1 citations · View on PubMed ↗

ITGBL1-MYH9 interaction in hepatic stellate cells acts as a mechano-regulator controlling liver fibrosis in mice.

The study investigated how the integrin β-like 1 (ITGBL1)–non-muscle myosin II (NM II)/actomyosin pathway regulates hepatic stellate cell (HSC) mechanotransduction and liver fibrosis in mice, with relevance to patient-activated HSCs. The authors found that ITGBL1 acts as a gatekeeper of HSC quiescence by negatively regulating actomyosin contractility-driven mechanotransduction, and that ITGBL1 is elevated in activated HSCs. This identifies ITGBL1 as a mechanoregulator and potential therapeutic target to limit cytoskeleton-driven HSC activation and fibrosis progression.

Li Y, Wang Y, Tong C et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

Ischemic Postconditioning in Patients With Acute Stroke With Successful Recanalization After Endovascular Therapy: A Pilot Randomized Controlled Trial.

This pilot randomized controlled trial tested whether ischemic postconditioning (IPostC) performed after successful recanalization reduces infarct growth in patients with acute ischemic stroke undergoing endovascular therapy. In a single-center, prospective, randomized, open-label design with blinded endpoint assessment, IPostC was evaluated as an adjunct to thrombectomy to mitigate ischemia-reperfusion injury. If effective, this strategy could provide a low-risk, procedure-adjacent intervention to improve outcomes beyond recanalization alone.

Xu Y, Zhang B, Liu S et al. · Stroke · (2026) · View on PubMed ↗

Sodium selenite attenuates sepsis-induced cardiac inflammation and oxidative injury by regulating TXN2/TXNIP/NLRP3 signaling and ferroptosis.

This study investigated how sodium selenite affects sepsis-induced cardiac inflammation and oxidative injury in the context of TXN2/TXNIP/NLRP3 signaling and ferroptosis, focusing on cardiomyocyte mitochondrial reactive oxygen species (mtROS) regulation. The key finding was that sodium selenite downregulated TXN2-induced mtROS, thereby attenuating inflammatory and oxidative damage in septic cardiomyopathy, and it implicated TXN2/TXNIP/NLRP3 pathway modulation alongside ferroptosis control. These results suggest a selenium-based therapeutic mechanism for protecting the heart during sepsis and provide targets for future translational studies.

Zhang L, Zhu D, Yu J · Frontiers in pharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Microprotein, macro-effect: DWORF as a therapeutic strategy in heart failure.

This article reviewed and proposed DWORF (dwarf open reading frame; gene name STRIT1) as a therapeutic strategy in heart failure by targeting the SERCA2a–phospholamban (PLN) regulatory axis. The central concept is that DWORF can enhance SERCA2a activity while avoiding the safety problems seen with strategies that fully disrupt PLN, where complete PLN loss is lethal in humans. If translated effectively, DWORF-based approaches could offer a more precise way to restore impaired SR Ca2+ cycling in failing myocardium.

Verry JP, Makarewich CA · Frontiers in cell and developmental biology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Kidney disease & transplantation outcomes

Natural History and Progression of Recurrent C3 Glomerulopathy and Primary Immune-Complex Membranoproliferative Glomerulonephritis in Kidney Transplantation.

This multinational retrospective cohort study examined the natural history and prognostic value of longitudinal kidney biomarkers in adults and children with biopsy-proven recurrent C3 glomerulopathy (C3G) or primary immune-complex membranoproliferative glomerulonephritis (IC-MPGN) after kidney transplantation. Across 48 centers in 11 countries, patients with recurrence and at least four serial measurements of eGFR and proteinuria were analyzed to define disease progression patterns and biomarker associations with graft outcomes. Clinically, the work aims to improve risk stratification and guide monitoring strategies for recurrent complement/immune-complex–mediated glomerular disease that commonly leads to graft loss.

Ruiz-Cabello JE, Yandian F, Torres IB et al. · Clinical journal of the American Society of Nephrology : CJASN · (2026) · View on PubMed ↗

---

Musculoskeletal, bone & fracture risk

Pregnancy- and lactation-associated osteoporosis: A position statement of the IAPM, IOF, ECTS, ESCEO, IMS, and EMAS.

This position statement reviewed evidence on pregnancy- and lactation-associated osteoporosis (PLO), focusing on recommended assessment, diagnosis, and treatment approaches for affected patients. PLO is characterized by fragility fractures—most often vertebral and sometimes multiple—occurring in late pregnancy or early postpartum, and the document synthesizes available study designs and safety considerations given limited comparative trials. Clinically, it provides a standardized framework to improve recognition and management of this rare but high-risk osteoporosis syndrome.

Hadji P, Athanasiadis A, Brandi ML et al. · International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · (2026) · View on PubMed ↗ · Free PDF ↗

Conceptual framework and expert guidance on intrapancreatic fat deposition: the Melbourne consensus.

This article is a consensus framework developed by 25 experts from 6 continents to standardize conceptual understanding and clinical assessment of intrapancreatic fat deposition (IPFD) using an iterative Delphi process. It produced 58 recommendations (30 unanimous; 28 with 90–99% agreement) addressing definitions, measurement approaches, and clinical implications across conditions such as pancreatitis, pancreatic cancer, and type 2 diabetes. The consensus is significant because it aims to harmonize how IPFD is evaluated in research and trials, enabling more comparable studies and clearer translation to patient care.

Petrov MS, Yamazaki H, Lu G et al. · Nature reviews. Gastroenterology & hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Global retinoblastoma service availability in 2024 and equity trends since 2017.

This international cross-sectional study with longitudinal comparison assessed global availability of retinoblastoma (Rb) diagnostic and treatment services in 2024 and evaluated equity trends since 2017 across 145 countries. In 2024, 438 Rb treatment centres participated, with 49 countries having no identified Rb centres (and four unconfirmed), and longitudinal analyses tracked changes in access to key diagnostics (CT, MRI, pathology, genetic testing) and treatments (intravenous, intravitreal, intra-arterial). The results highlight persistent geographic and income-related gaps in Rb care, supporting policy and investment to expand diagnostic capacity and evidence-based treatment delivery.

The British journal of ophthalmology · (2026) · View on PubMed ↗ · Free PDF ↗

Breast Cancer Follow-Up and Surveillance After Primary Treatment: ASCO Guideline Update.

This ASCO guideline update studied evidence and expert consensus to develop recommendations for breast cancer follow-up and surveillance after primary treatment in patients with early-stage disease. It found limited direct randomized evidence comparing different follow-up strategies by relapse risk, leading to modified Delphi consensus-based recommendations and a mammography guideline grounded in a single randomized trial. The significance is standardized, risk-informed surveillance guidance for clinicians to balance detection of recurrence with avoidance of low-value testing.

Nahleh Z, Alfano CM, Somerfield MR et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Hip Fractures: A Review.

This narrative review summarized epidemiology, classification, and outcomes of hip fractures, including intracapsular versus extracapsular patterns and mortality and functional recovery after fracture. The key finding is that hip fractures carry substantial short-term mortality (median 1-year mortality ~22%) and that recovery of basic activities of daily living is variable (often 42%–71% by 6 months), with common fracture distributions such as intertrochanteric fractures (~48%). Scientifically and clinically, the review consolidates risk and outcome expectations to inform prevention, triage, and management strategies for older adults sustaining hip fractures.

Johannesdottir F, Roberts JE, Kiel DP et al. · JAMA · (2026) · View on PubMed ↗

---

Aging, climate/exposures & systemic inflammation

Skin-innervating glutamatergic neurons modulate aging.

This study examined how skin-innervating glutamatergic neurons regulate skin aging in mice, focusing on neurofilament heavy chain (Nefh) in Vglut2+ neurons and its effects on dermal fibroblasts. Cutaneous denervation and Nefh deletion in Vglut2+ glutamatergic neurons accelerated skin aging by inducing fibroblast senescence and collagen loss, while glutamate supplementation improved aging phenotypes. These findings identify a neuron–fibroblast signaling axis (Nefh/Vglut2+ glutamatergic neurons and glutamate) as a mechanistic target to modulate age-related skin degeneration.

Wang Z, Jin X, Wu Y et al. · Cell · (2026) · View on PubMed ↗

Interleukin-18 armours antitumour immune effectors.

This preclinical study investigated how hematopoietic stem cell (HSC) aging drives aging-associated inflammation via trained immunity in mice, focusing on the mitochondrial deacetylase SIRT3. SIRT3 suppressed maladaptive trained immunity by reducing the aging-associated HSC response, and SIRT3 overexpression in HSCs improved HSC function and attenuated functional decline in distant tissues. These results link a specific metabolic regulator (SIRT3) to the origin of chronic inflammation and suggest a potential intervention point to mitigate systemic aging phenotypes.

Sharma A, Bishara GG, Olejniczak SH et al. · Nature reviews. Immunology · (2026) · View on PubMed ↗

Effect of low-dose naltrexone for long COVID: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated randomized controlled trials and pre-post studies of low-dose naltrexone (LDN) for long COVID symptoms, including fatigue, quality of life, cognitive symptoms, and function, with searches through 5 May 2026. The study synthesized available evidence on whether LDN improves long COVID outcomes compared with control, drawing conclusions about efficacy and safety across included trials. Scientifically and clinically, it clarifies the current evidence base for LDN as a potential symptom-modifying therapy in long COVID and identifies gaps for future well-powered trials.

Byambasuren O, Atkins T, Baptista S et al. · BMJ open · (2026) · View on PubMed ↗ · Free PDF ↗

Vitamin C attenuates primate bone marrow aging at the molecular and progenitor level.

This study mapped single-cell transcriptomic changes during primate bone marrow aging and tested whether long-term oral vitamin C (VC) supplementation modifies aging at the molecular and progenitor-cell levels. VC partially attenuated age-associated declines by expanding the common lymphoid progenitor (CLP) pool and rebalancing hematopoietic stem and progenitor (HSPC) lineage commitment trajectories, countering aging-driven CLP depletion and myeloid-biased output. These findings support vitamin C as a potentially modifiable intervention to preserve immune function during primate bone marrow aging.

Ye Y, Zhang H, Xin Z et al. · Cell stem cell · (2026) · View on PubMed ↗

Tidying up aging organs.

This Science commentary highlights a mechanism of organ aging involving prostaglandin signaling that affects macrophage clearance of toxic neutrophils. The key finding emphasized is that a specific prostaglandin pathway can prevent macrophages from performing efferocytosis of senescent/toxic neutrophils, thereby promoting age-related decline. The significance is that targeting this prostaglandin-driven macrophage dysfunction could be a therapeutic strategy to slow or reverse aspects of aging-related organ deterioration.

FitzGerald GA · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Restored clearance of senescent neutrophils by tissue-resident macrophages limits organ aging.

This study examined how tissue-resident macrophages (TRMs) regulate age-related organ decline by clearing senescent neutrophils, focusing on the immunomodulatory prostaglandin E2 (PGE2) receptor EP2. In aged mice, reducing TRM EP2 signaling preserved youthful mitochondrial fitness and prevented cognitive decline, frailty, sarcopenia, adiposity, cardiac impairment, and systemic inflammation, with plasma proteomics implicating the liver as a major source of age-associated immune changes. The significance is that restoring TRM-mediated neutrophil efferocytosis via EP2 modulation can limit systemic inflammation and multiple organ aging phenotypes, suggesting a tractable immunometabolic intervention.

Tan YJ, Conley TE, Yao F et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗

Body Mass Index and Risks of More Than 40 Cause-Specific Mortality in Chinese Women: A Prospective Cohort Study.

This prospective cohort study analyzed the association between body mass index (BMI) across the full spectrum and cause-specific mortality in 262,704 Chinese women aged 30–79 from the China Kadoorie Biobank. Compared with a reference BMI of 22.5–23.9, both underweight and higher BMI categories were associated with increased risks of mortality from multiple causes, with particular emphasis on low BMI and premature versus nonpremature death. The results support BMI-informed risk stratification for women and highlight underweight as a clinically important, modifiable risk factor for early mortality.

Hu J, Ke Y, Yu C et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Heatwave Exposure Accelerates Biological Aging via Metabolic Dysregulation.

This study used the China Health and Retirement Longitudinal Study (CHARLS) to test whether heatwave exposure in the 12 months before biological age assessments (2011 and 2015) accelerates biological aging in middle-aged and older adults. Using the Klemera–Doubal method to estimate biological age and compute biological age acceleration (BAA), it found that heatwave exposure was associated with more rapid biological aging via metabolic dysregulation. These findings link climate-related heat exposure to measurable aging biomarkers and highlight metabolic pathways as potential mediators for risk reduction.

Xu D, Li D, Chen Y et al. · Cyborg and bionic systems (Washington, D.C.) · (2026) · View on PubMed ↗ · Free PDF ↗

---

---

Generated automatically on July 18, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.