PubMed Trending Research Digest — August 07, 2026

Automated digest · 99 articles · 15 research areas · August 07, 2026

Overview

Across this week’s set of papers, a dominant theme is the move toward more realistic, context-aware models for biology and therapy—especially in oncology. Multiple studies expand patient-derived resources (next-generation patient-derived cancer models, organoid biobanks, and 3D model CRISPR/multi-omics profiling) to better capture tumor heterogeneity and subtype-specific vulnerabilities. Complementing these model-building efforts, several mechanistic and translational cancer papers focus on how the tumor microenvironment shapes response: spatially organized immune changes under immunosuppression, extracellular vesicle-driven premetastatic macrophage activation, neutrophil metabolic reprogramming, and lactylation-associated immune-excluded states. Together, these works emphasize that “what the tumor is” and “what the immune system is doing” must be measured in the right spatial and temporal context to predict and improve treatment outcomes.

A second major thread links immune regulation to disease risk and therapeutic opportunity beyond classic oncology. Studies span trained immunity (BCG-derived HSP70 as a defined alternative), astrocyte-driven antigen presentation in CNS autoimmunity, glial contributions to neuroinflammation and delirium, and immune trajectory modeling during transplant immunosuppression withdrawal. Infectious disease papers add mechanistic depth—mapping viral reactivation dynamics in COVID-19, defining host regulatory axes in severe viral pneumonia, and characterizing immune-escape epitope classes on SARS-CoV-2 NTD—while also highlighting how host pathways (e.g., macrophage effector regulation via TREM2) determine outcomes.

Finally, several studies converge on metabolic/epigenetic control systems as actionable levers across organ systems: lipid and energy-state genetics (FNIP1–TG:HDL), stress-driven epitranscriptomic regulation in esophageal cancer, lactylation and IL-6 interorgan signaling in diabetes, and chromatin/translation mechanisms (TF access, m7G cap biology, mitochondrial translational control). In parallel, clinical and translational work continues to refine real-world decision-making—through comparative effectiveness studies, trial designs aimed at reducing treatment burden, and risk models—while computational and bioengineering advances (foundation models for spatial proteomics, AI-guided cfDNA tissue-of-origin inference, and AI-designed bacteriophages) aim to make complex biological measurement more scalable and clinically usable.

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Cancer models & functional genomics (organoids/DepMap/CRISPR screens)

Zhigancao decoction ameliorates ischemic heart failure-related ventricular arrhythmias through attenuation of transforming growth factor-β/Smad-associated myocardial fibrosis.

Zhigancao decoction (ZGCT/Fumai Decoction) was studied in an ischemic heart failure model to determine how it affects ventricular arrhythmias and myocardial fibrosis, focusing on the TGF-β/Smad signaling pathway. ZGCT ameliorated ischemic heart failure–related ventricular arrhythmias by attenuating TGF-β/Smad-associated myocardial fibrosis. These findings support ZGCT as a potential adjunct therapy targeting TGF-β/Smad-driven fibrotic remodeling to reduce arrhythmia risk in ischemic heart failure.

Wang X, Zhou L, Ding H et al. · Journal of ethnopharmacology · (2026) · View on PubMed ↗

Coixol attenuates Ulcerative Colitis by modulating the ILC3 response via the Wnt/β-catenin pathway.

Coixol was evaluated in ulcerative colitis models to define its mechanism of action on innate lymphoid cell type 3 (ILC3) responses, with emphasis on the Wnt/β-catenin pathway. Coixol attenuated ulcerative colitis by modulating ILC3 activity through regulation of Wnt/β-catenin signaling. This mechanistic link suggests Coixol may be a targeted anti-inflammatory strategy for UC by reprogramming ILC3-driven intestinal immune responses.

Ma J, Yin Q, Zhou Y et al. · Journal of ethnopharmacology · (2026) · View on PubMed ↗

Prospective study of efgartigimod in severe myasthenia gravis exacerbations requiring ventilatory or enteral support.

Efgartigimod was studied in 16 adults with severe generalized myasthenia gravis (AChR- or MuSK-antibody positive) experiencing exacerbations requiring ventilatory or enteral support in a prospective, single-arm, open-label trial. The study assessed safety and clinically meaningful improvement in myasthenia gravis activities of daily living, with outcomes reported for patients meeting impending myasthenic crisis criteria. If efficacy and safety are confirmed, efgartigimod could become an important treatment option for severe MG exacerbations requiring life-support-level care.

Shelly S, Rosenberg A, Zoabi M et al. · Journal of neuromuscular diseases · (2026) · View on PubMed ↗

A tumour-derived organoid biobank maps cancer gene dependencies.

This study created and characterized a tumor-derived organoid biobank to map cancer gene dependencies across clinically annotated patient models. Using whole-genome and transcriptome sequencing plus genome-wide CRISPR-Cas9 screens across 162 organoids spanning colorectal, oesophageal, ovarian, pancreatic, and gastric cancers, the biobank linked organoid phenotypes to patient tumor context while maintaining genetic stability. Providing renewable, genetically stable organoid models with dependency maps improves the translational relevance of functional genomics for identifying actionable cancer vulnerabilities.

Herranz-Ors C, Bhosle SG, Beck AE et al. · Nature · (2026) · View on PubMed ↗

A compendium of next-generation patient-derived models for diverse cancers.

This Nature report describes the Human Cancer Models Initiative, generating 665 next-generation patient-derived cancer models from 2,780 donors across 25 cancer types to assess whether models retain key properties of original patient tumours during long-term expansion. The compendium provides a large, diverse resource of next-generation patient-derived models (including organoid-like systems) designed to better capture cancer heterogeneity than existing model collections. Scientifically, it enables more representative mechanistic studies and therapeutic testing across many tumour types and patient backgrounds.

ElHarouni D, Al-Jazrawe M, Choi S et al. · Nature · (2026) · View on PubMed ↗

A dependency map enhanced with next-generation 3D cancer models.

This study enhanced the Cancer Dependency Map (DepMap) by performing 147 genome-scale CRISPR screens and multi-omic profiling in next-generation 3D cancer models to map cancer vulnerabilities beyond traditional 2D cell lines. The authors report that next-generation models improve subtype representation and yield dependency and multi-omic signals that better reflect perturbation responses relevant to specific tumour contexts. This supports more accurate identification of actionable therapeutic targets for precision oncology.

Neiswender JV, Maffa S, Brenan L et al. · Nature · (2026) · View on PubMed ↗

Functional profiling of ovarian cancer models reveals Bcl-xL/NOTCH targeting to overcome resistance.

This NPJ Precision Oncology study created 35 patient-derived ovarian cancer models from 22 patients to functionally profile vulnerabilities underlying platinum resistance and chemoresistance. It identified Bcl-xL and NOTCH pathway targeting as a strategy to overcome resistance in these models. The work supports patient-specific therapeutic selection by linking functional dependencies to actionable combination targets in resistant ovarian cancer.

Gudoityte G, Berkovska O, Orre LM et al. · NPJ precision oncology · (2026) · View on PubMed ↗

let-7 miRNA and lin-46 mRNA are essential targets of the LIN28 RNA-binding protein in Caenorhabditis elegans developmental timing regulation.

This study investigated LIN28 RNA-binding protein function in Caenorhabditis elegans developmental timing regulation by testing whether specific LIN28-bound RNAs are essential targets. Loss of LIN28 left most LIN28-bound transcripts unchanged, but genetic analyses identified let-7 miRNA and lin-46 mRNA as the functionally essential LIN28 targets. The findings provide direct evidence that LIN28’s broad RNA binding can converge on a small set of critical effectors to control developmental timing.

Brunner J, Neagu A, Gaidatzis D et al. · PLoS biology · (2026) · View on PubMed ↗

TAK1 operates at the primary cilium in non-canonical TGFB/BMP signaling to control heart development.

This study examined how TAK1 (MAP3K7) functions at the primary cilium in non-canonical TGFB/BMP signaling to control heart development, using genetic and mechanistic experiments in zebrafish and cell models. Zebrafish tak1 and tab2 mutants showed cardiac and extracardiac developmental defects, and tak1 mutant hearts exhibited downregulation of core cardiac transcriptional programs. The work links ciliary localization of TAK1 signaling to congenital heart disease mechanisms, supporting TAK1 as a key regulator of developmental gene control in non-canonical TGFB/BMP pathways.

Doganli C, Thomsen OK, Baird DA et al. · PLoS biology · (2026) · View on PubMed ↗

Prognostic risk modeling based on integrated multi-omics analysis identifies CRY2 as a key regulator in tumor immunity and patient survival in colorectal cancer.

This study developed a prognostic risk model for colorectal cancer (CRC) using integrated multi-omics data to identify CRY2 as a key regulator in tumor immunity and patient survival. Using TCGA-COAD and GSE39582 cohorts, WGCNA and machine-learning methods (forward stepwise Cox regression with Random Survival Forest) produced a ferroptosis- and lipid metabolism–linked signature in which CRY2 emerged as a central driver associated with survival and immune features. The model provides a data-driven framework for CRC prognosis and highlights CRY2 as a potential target connecting metabolic regulation, ferroptosis biology, and anti-tumor immunity.

Guo Y, Zou Y, Wang M · Annals of medicine · (2026) · View on PubMed ↗

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Cancer immunology & tumor microenvironment (incl. EVs, macrophages, neutrophils)

Tumoral extracellular vesicles and particles reprogram interstitial macrophages in the lung to promote vascular permeability and metastasis.

This study examined how tumor-derived extracellular vesicles and particles (EVPs) reprogram lung interstitial macrophages in female mice to promote vascular permeability and metastasis. EVPs rapidly activated NF-κB and JAK-STAT signaling in interstitial macrophages, driving IL-6 secretion and vascular leakiness within 1 hour, and macrophage depletion markedly reduced EVP-induced leakiness and metastasis. Identifying extracellular vesicle-associated integrin α5 (ITGα5) as a major mediator links a specific EVP component to a macrophage-driven premetastatic niche mechanism that could be therapeutically targeted to limit metastatic seeding.

Dror S, Wortzel I, Lucotti S et al. · Nature cancer · (2026) · View on PubMed ↗

ZFP36L2 orchestrates stress-adaptive plasticity in regeneration and cancer.

This study examined how the RNA-binding protein ZFP36L2 regulates stress-adaptive phenotypic plasticity during intestinal regeneration and colorectal cancer (CRC) metastasis. In mouse colon regeneration and CRC contexts, ZFP36L2 ablation blocked dedifferentiation into an intestinal stem cell (ISC) state, reduced ISC gene expression/function, and impaired regeneration, while human CRC data linked ZFP36L2 loss to altered dedifferentiation programs. Establishing ZFP36L2 as a pivotal stress-responsive switch connects a specific gene to dynamic cell-fate reprogramming, suggesting it as a potential target to modulate regenerative and metastatic plasticity.

Jiang Q, Raghavan MS, Rodriguez AM et al. · Nature · (2026) · View on PubMed ↗

Spatial biology reveals altered macrophage states in immunosuppressed non-melanoma skin cancer.

This Cell study used integrated single-cell sequencing, spatial transcriptomics, multiplex immunofluorescence, and spatial epigenomic profiling to compare tumour immune microenvironments in immunocompetent versus immunosuppressed patients with non-melanoma skin cancer. Immunosuppressed tumours showed reduced intratumoral macrophage densities and altered spatial organization and T-cell clonality, despite largely preserved overall immune-cell composition. These findings identify spatially distinct macrophage and T-cell state changes associated with systemic immunosuppression, informing strategies to improve immunotherapy responsiveness.

Naara S, Kochat V, Rao X et al. · Cell · (2026) · View on PubMed ↗

Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.

This article is a mechanistic review summarizing how immune cell migration into tumors and inflammatory sites is controlled by molecular guidance systems, including chemokine/cytokine receptor pairs and adhesion pathways, and how immune reservoirs such as tertiary lymphoid structures, bone marrow, and the intestine act as mobilization hubs. It highlights therapeutic targets aimed at modulating these migration programs to improve immune infiltration and function in cancer and inflammatory disease. The synthesis provides a roadmap for developing anti-migration or pro-infiltration strategies that could enhance immunotherapy efficacy and control chronic inflammation.

Lu Y, Shao D, Xiao Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

ITPKB suppresses ER calcium release to promote CXCL9 expression and enhance immunotherapy sensitivity in triple-negative breast cancer.

The study examined the role of inositol-trisphosphate 3-kinase B (ITPKB) in triple-negative breast cancer (TNBC) by analyzing human TNBC tissues with single-cell RNA sequencing (scRNA-seq) and testing ITPKB ectopic expression. ITPKB increased secretion of the T-cell–recruiting chemokine CXCL9 and enhanced sensitivity to immunotherapy by promoting cytotoxic T lymphocyte trafficking into the tumor microenvironment (TME). This mechanistic link between ITPKB and CXCL9 provides a potential target to reverse immunotherapy resistance in TNBC.

Zhang K, Wang X, Yi Q et al. · Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · (2026) · View on PubMed ↗

Disrupting galectin-3 and NET-mediated microglia-neutrophil cross-talk suppresses pathological retinal angiogenesis.

This study combined integrative single-cell RNA sequencing of human fibrovascular retinal membranes with multicohort clinical datasets to define immune-angiogenic mechanisms in diabetic retinopathy and then tested therapeutic disruption of galectin-3 and NET-mediated microglia–neutrophil cross-talk. Neutrophil infiltration independently predicted diabetic retinopathy progression, and mechanistically activated microglia promoted neutrophil infiltration via secreted factors, with galectin-3/NET signaling driving pathological retinal angiogenesis. Targeting galectin-3 and NET-mediated microglia–neutrophil communication may provide an immune-vascular therapeutic approach to suppress vision-threatening neovascularization.

Zhou Z, Yuan T, Sun J et al. · Science translational medicine · (2026) · View on PubMed ↗

Biophysical reprogramming of immunosuppressive neutrophils by cold atmospheric plasma reinvigorates antitumor immunity.

The study tested whether cold atmospheric plasma (CAP) can biophysically reprogram tumor-associated immunosuppressive neutrophils to restore antitumor immunity. CAP delivered reactive oxygen species and redox cues that inhibited mitophagy, restored mitochondrial membrane potential and oxidative metabolism, and shifted neutrophils from immunosuppressive toward immunostimulatory function. This supports CAP as a non-pharmacologic immunotherapy strategy targeting neutrophil metabolic control pathways in cancer.

Wang G, Cui Z, Jiang X et al. · Science advances · (2026) · View on PubMed ↗

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Cancer therapeutics & resistance (drugs, combinations, targeted therapy, vaccines/antibodies)

Talquetamab in patients with relapsed/refractory multiple myeloma: 3-year follow-up of the phase 1/2 MonumenTAL-1 study.

Talquetamab, a GPRC5D-targeting bispecific antibody, was followed for 3 years in patients with relapsed/refractory multiple myeloma in the phase 1/2 MonumenTAL-1 study, including cohorts with and without prior T-cell redirection therapy (TCR). Across talquetamab dosing schedules (0.4 mg/kg weekly and 0.8 mg/kg every other week) and a prior-TCR cohort, the study reported durable efficacy with overall response rates in the ~67–74% range and ongoing safety. Long-term results support talquetamab’s sustained clinical activity as a GPRC5D-directed therapy for R/R multiple myeloma.

Rasche L, Schinke C, Touzeau C et al. · Blood · (2026) · View on PubMed ↗

Targeting GEM Reprograms Macrophages and Overcomes Immunotherapy Resistance in Esophageal Squamous Cell Carcinoma.

GTP-binding protein overexpressed in skeletal muscle (GEM) was investigated as a tumor-intrinsic driver of immunotherapy resistance in esophageal squamous cell carcinoma (ESCC), focusing on how GEM alters tumor-associated macrophages (TAMs) and CD8+ T-cell infiltration. GEM expression promoted SERPINE1 secretion that acted on macrophage LRP1 to induce alternative macrophage activation and suppress antitumor immunity, reducing response to anti–PD-L1 therapy. Targeting the GEM–SERPINE1–LRP1 axis may overcome PD-L1 immunotherapy resistance by reprogramming TAM-mediated immunosuppression in ESCC.

Wu L, Ren C, Zhang Y et al. · Cancer research · (2026) · View on PubMed ↗

Membranolytic peptide programs immunogenic cell death for cancer therapy.

This study developed a synthetic-acid-responsive membranolytic peptide (aMP), aMPC16-CA50, to induce immunogenic membranolytic cell death (mLCD) in tumor cells and evaluated its therapeutic impact. The peptide triggered a time-lagged rupture program from lysosomal to plasma membranes, activated an inflammatory transcriptional program, and robustly potentiated immune checkpoint blockade therapy. Programming a specific, pH-responsive cell death mode offers a rational strategy to enhance antitumor immunity and improve the efficacy of checkpoint inhibitors.

Yuan Y, Liang L, Li J et al. · Nature · (2026) · View on PubMed ↗

Development of an investigational medicinal stem cell gene therapy product to attempt curing human immunodeficiency virus infection.

This Scientific Reports study focused on developing an investigational medicinal stem cell gene therapy product intended to attempt curing HIV infection by leveraging CCR5 deletion strategies. The approach is motivated by the “Berlin patient” observation that allogeneic stem cell transplantation from a CCR5Δ32/Δ32 donor enabled long-term remission without antiviral therapy, and it translates this concept to autologous stem cell gene therapy with CCR5 disruption. If successful, it could provide a pathway toward durable HIV eradication while avoiding T-cell depletion.

Weigand L, Herkt S, Voges M et al. · Scientific reports · (2026) · View on PubMed ↗

Targeting a novel metabolic vulnerability of non-small cell lung cancer to fatty acid oxidation surmounts chemoresistance.

The study investigated how C/EBPβ alternative translational isoforms (LAP and LIP) rewire metabolism in non-small cell lung cancer (NSCLC) cells to drive chemoresistance to platinum drugs, using LAP- or LIP-overexpressing NSCLC models. LAP/LIP-dependent metabolic reprogramming increased chemoresistant traits associated with ABC efflux transporter expression and function, identifying fatty acid oxidation as a metabolic vulnerability that can be targeted to overcome platinum resistance. These findings suggest a gene-isoform–linked metabolic mechanism (C/EBPβ LAP:LIP) and support fatty acid oxidation targeting as a strategy to improve outcomes in platinum-resistant NSCLC.

Fontana S, Belisario DC, Giannotta C et al. · Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · (2026) · View on PubMed ↗

Vorasidenib improves response to subsequent chemoradiation in a genetically engineered mouse model of IDH-mutant glioma.

This work tested whether upfront exposure to the mutant IDH1/2 inhibitor vorasidenib (mIDHi) alters the efficacy of subsequent chemoradiation in a genetically engineered mouse model of IDH-mutant glioma. The study found that vorasidenib improved outcomes when followed by chemoradiation after progression compared with chemoradiation alone. Clinically, it supports sequencing vorasidenib with standard chemoradiation as a strategy to enhance durable control in IDH-mutant glioma.

Shi DD, Calvo Fernández E, Puliyappadamba VT et al. · Science translational medicine · (2026) · View on PubMed ↗

Development of a structurally distinct TopBP1 inhibitor that enhances PARP blockade and reverses osimertinib resistance.

This study used docking-guided screening and structure–activity relationship optimization to develop CS18, a structurally distinct TopBP1 BRCT7/8 inhibitor, and tested its ability to enhance PARP blockade and reverse osimertinib resistance. CS18 selectively disrupted TopBP1-BRCT7/8 interactions and, in combination with PARP inhibition, improved anti-tumor effects while counteracting resistance to the EGFR inhibitor osimertinib. The work supports TopBP1 BRCT7/8 inhibition as a rational combination strategy to overcome targeted-therapy resistance in cancers with TopBP1-driven stress/replication signaling.

Lin FT, Lin SJ, Liu K et al. · Science advances · (2026) · View on PubMed ↗

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Cancer genomics & molecular classification (subtypes, biomarkers, multi-omics signatures)

Multi-omics integration unravels four molecular subgroups of corticotroph pituitary neuroendocrine tumours with distinct clinicopathological features.

This Nature Communications study integrated epigenome, transcriptome, and proteome data from 270 corticotroph pituitary neuroendocrine tumours (111 internal and 159 external) to define molecular subgroups. The authors identified four robust molecular subgroups with distinct clinicopathological features. This molecular classification improves biological stratification of corticotroph PitNETs and may guide more tailored prognostic assessment and treatment development.

Dottermusch M, Ryba A, Gocke A et al. · Nature communications · (2026) · View on PubMed ↗

Influence of KRAS mutation subtypes on response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer: meta-analysis.

This meta-analysis studied whether different KRAS mutation subtypes influence pathological complete response (pCR) rates after neoadjuvant chemoradiotherapy in locally advanced rectal cancer (LARC). Across included studies, the analysis pooled odds ratios for KRAS mutation subtypes with respect to pCR using a random-effects model, aiming to determine whether specific KRAS variants predict treatment response. Clinically, identifying KRAS subtype–specific response patterns could improve risk stratification and guide selection of neoadjuvant strategies in LARC.

Sadien ID, Cooper G, Phillips V et al. · BJS open · (2026) · View on PubMed ↗

Pan-cancer multi-omics machine learning defines a lactylation-associated immune-excluded tumor state with proteomic and experimental corroboration.

This pan-cancer study used multi-omics machine learning on 9712 TCGA tumors across 33 cancer types (integrated with GTEx, multiple GEO cohorts, and an institutional clear-cell renal cell carcinoma cohort) to define a lactylation-associated immune-excluded tumor state, with proteomic corroboration using DIA-NN. The analysis identified a recurrent lactylation-associated program that characterizes immune-excluded tumors and implicated hsa-miR-431-5p as a functional component, supported by immune deconvolution, TIDE, and SHAP-based modeling plus experimental/proteomic validation. The work provides a lactylation-linked biomarker framework for recognizing immune-excluded phenotypes and potentially stratifying patients for immunotherapy.

Bo Z, Zhang S, Zheng Z et al. · Computational biology and chemistry · (2026) · View on PubMed ↗

Chronic Stress-Induced m7G Cap Modification of ADRB2 Dysregulates the Pentose Phosphate Pathway to Promote Esophageal Squamous Cell Carcinoma Progression.

The study examined how chronic stress-induced N7-methylguanosine (m7G) cap modification of ADRB2 dysregulates metabolism to promote esophageal squamous cell carcinoma (ESCC) progression, integrating patient serum metabolomics with mechanistic signaling experiments. Chronic stress features in ESCC patients associated with elevated epinephrine and pentose phosphate pathway (PPP) enrichment, and β2-adrenergic receptor (ADRB2) signaling stabilized MYCBP by displacing VHL, enhancing MYC transcriptional activity and upregulating PPP enzymes. This connects stress-driven epitranscriptomic regulation of ADRB2 to MYC–PPP metabolic reprogramming, highlighting potential targets to counteract stress-associated tumor progression.

Zhang Z, Liu F, Wang P et al. · Cancer research · (2026) · View on PubMed ↗

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Non-cancer cardiometabolic disease (diabetes, lipids, atherosclerosis, kidney protection)

Association of Enlarged Perivascular Spaces and Total Small Vessel Disease Burden With Kidney Function.

Enlarged perivascular spaces (EPVS) in the basal ganglia (BG-EPVS) and centrum semiovale (CSO-EPVS) were analyzed in pooled individual patient data from the Microbleeds International Collaborative Network to test associations with kidney function, including reduced eGFR and glomerular hyperfiltration. The study evaluated whether EPVS burden correlates with eGFR abnormalities, extending prior work that focused mainly on reduced kidney function. Establishing EPVS–kidney links would strengthen the concept of shared small-vessel pathology across brain and kidney and could inform risk stratification after ischemic stroke/TIA.

Nash PS, Ambler G, Best JG et al. · Neurology · (2026) · View on PubMed ↗

FNIP1 variants are associated with favourable metabolism in 1 million humans.

This study used exome sequencing in 1,032,116 people from America, Europe, and Asia to test associations between rare protein-coding variants in FNIP1 and the triglyceride-to-HDL cholesterol (TG:HDL) biomarker of energy state. FNIP1 variants were associated with a favourable metabolic profile, including lower TG:HDL and links to reduced cardiometabolic risk factors and diseases. These findings strengthen the genetic basis for energy metabolism and highlight FNIP1 as a potential target for cardiometabolic risk reduction.

Hindy G, Adam RC, Sosina O et al. · Nature · (2026) · View on PubMed ↗

Morroniside ameliorates hepatic fibrosis in mice by targeting ACYP1 to promote NCOA4-mediated ferritinophagy and ferroptosis.

The study tested whether morroniside, an iridoid glycoside, ameliorates carbon tetrachloride (CCl4)- and Gubra Amylin NASH (GAN)-induced hepatic fibrosis in mice by targeting ACYP1 and promoting NCOA4-mediated ferritinophagy and ferroptosis. Morroniside reduced liver fibrogenesis and mechanistically increased ferritinophagy/ferroptosis signaling through an ACYP1-dependent pathway involving NCOA4. These results support morroniside as a candidate anti-fibrotic agent and highlight ACYP1–NCOA4 ferritinophagy–ferroptosis as a therapeutic axis.

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

Periodontitis, epicardial adipose tissue and coronary events: the Swedish Cardiopulmonary Bioimage Study.

This study used SCAPIS (Swedish CArdioPulmonary bioImage Study) linked with national dental and coronary heart disease registers to test whether subclinical atherosclerosis mediates the association between periodontitis and incident CHD and whether periodontitis phenotypes relate to coronary atherosclerosis and epicardial adipose tissue (EAT) attenuation. Coronary atherosclerosis was quantified using coronary artery imaging (as described in the methods), and EAT attenuation was evaluated as an inflammation marker. The work is significant because it targets a mechanistic pathway—subclinical atherosclerosis and inflammation—linking periodontal disease to future coronary events.

Teleka S, Persson P, Vähäsarja N et al. · European heart journal · (2026) · View on PubMed ↗

USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis.

This study used single-cell RNA sequencing and human atherosclerotic plaque validation to define mechanisms driving vascular smooth muscle cell (VSMC) senescence, focusing on TGFBR1 and its regulation by the deubiquitinase USP5 in human lesions and Apoe-deficient mice. TGFBR1 was enriched in senescent VSMCs, VSMC-specific TGFBR1 knockin accelerated plaque development and increased VSMC senescence, and USP5 stabilized TGFBR1 by removing K48-linked polyubiquitin. These results implicate the USP5–TGFBR1 axis as a mechanistic driver of atherosclerosis and a potential therapeutic target to limit VSMC senescence.

Cui X, Hu Y, Lin L et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

U-Shaped Association Between Left Ventricular Dimension and Mortality in Patients With Heart Failure.

This nationwide cohort study investigated the association between left ventricular dimension and mortality in heart failure patients using data from the Chinese Cardiovascular Association Database-Heart Failure Center Registry. In a large real-world population enrolled from 2018 to 2022, the relationship between left ventricular size and mortality was U-shaped, indicating increased risk at both smaller and larger dimensions beyond the confounding influence of ejection fraction. These findings refine prognostic risk stratification using left ventricular structural measurements in routine clinical practice.

Wang H, Zhang L, Ji C et al. · JAMA cardiology · (2026) · View on PubMed ↗

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Neurodegeneration & neuroinflammation (ALS/FTD/PD/AD/delirium/stress neurobiology)

Neuroinflammation as molecular landscape of post-operative delirium revealed by live human brain multi-omics profiling.

This study investigated the molecular basis of post-operative delirium (POD) by performing live human brain multi-omics profiling in patients undergoing neurosurgery. Single-nucleus RNA sequencing identified POD-specific transcriptional alterations, with prominent neuroinflammatory signatures in glial cells—especially microglia—and additional astrocyte changes in synaptic and migratory pathways. Defining a live-brain neuroinflammation molecular landscape in humans provides a scientific basis for developing glia-targeted biomarkers and interventions to reduce POD risk and its long-term cognitive consequences.

Ishii T, Wang T, Shibata K et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Amygdala astrocyte primary cilium mechanisms contribute to stress behaviours.

This study investigated how primary cilia in amygdala astrocytes contribute to stress-related behaviors. It found that amygdala astrocytes show stress-associated reductions in primary-cilium-related gene/protein expression and exhibit shortened primary cilia, and that astrocyte signaling mechanisms involving primary cilia and GPCR pathways likely mediate behavioral effects. Linking astrocyte primary cilium biology to stress behaviors provides a mechanistic framework for understanding how adverse experiences reshape neural regulation.

Pelaz SG, Mitsui K, Kolosowska N et al. · Nature · (2026) · View on PubMed ↗

Recent Advances in Autophagy and Immunotherapy for the Clearance of Aggregated α-Synuclein in Parkinson’s Disease.

This review synthesized recent evidence on autophagy and immunotherapy strategies aimed at clearing aggregated α-synuclein in Parkinson’s disease, emphasizing the autophagy-lysosomal pathway as a primary route for aggregated/oligomeric species. It highlights that mutations in SNCA worsen α-synuclein aggregation and impair clearance, and it discusses therapeutic approaches that promote autophagosome formation (including via AMPK) and complementary immunotherapies targeting toxic α-synuclein. The review supports targeting aggregated α-synuclein clearance mechanisms—particularly autophagy-lysosomal pathways—as a rational therapeutic direction for Parkinson’s disease.

Jannat K, Lee SB, Jung HR et al. · Aging and disease · (2025) · View on PubMed ↗

Early and Divergent Lipid Mediator Remodelling in Fast Versus Slow Skeletal Muscles of Female hSOD1G93A Mice.

This study characterized early and muscle-type-specific remodeling of the endocannabinoid system (ECS) in female hSOD1G93A transgenic mice versus nontransgenic littermates at presymptomatic and symptomatic ages, using endocannabinoid and N-acyl-ethanolamine profiling. It found that ECS lipid mediator changes differed over time and between fast and slow skeletal muscles in the ALS model. These results suggest that ECS dysregulation is an early, compartmentalized feature of ALS skeletal muscle pathology and may represent a targetable pathway for preserving muscle function.

Dalle S, Vanderbeke K, Burg T et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗

Glial cell toxicity in a Drosophila C9orf72 neurodegeneration model.

The study examined glial contributions to neurodegeneration in a Drosophila model of C9orf72 G4C2 repeat expansion by using glial cell type-specific expression of dipeptide repeats (DPRs), repeat-only RNA, or related constructs. Glial expression of specific C9orf72 repeat-derived toxic species produced neurodegenerative phenotypes, indicating that glia can drive or amplify pathology beyond neuron-autonomous effects. This clarifies cell-type-specific mechanisms of C9orf72 repeat expansion toxicity and supports targeting glial pathways in ALS/FTD.

Hubbard I, Dubnau J · PLoS genetics · (2026) · View on PubMed ↗

A single-domain antibody targets aggregation-prone region of α-synuclein to reduce synucleinopathy, rescue neurodegeneration and improve function.

This preprint study developed single-domain antibodies (sdAbs) against an aggregation-prone region of α-synuclein (α-syn) and tested whether they can reduce synucleinopathy-related pathology in vivo. The authors report that an sdAb targeting the aggregation-prone region can reduce α-syn aggregation, rescue neurodegeneration, and improve functional outcomes in a mouse model, building on prior evidence of acute α-syn clearance and diagnostic imaging potential. If validated, this approach could provide a targeted immunotherapy strategy to slow α-syn–driven neurodegeneration in synucleinopathies.

Pragati, Congdon EE, Jiang Y et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗

Astrocyte reactivity modifies the effects of locus coeruleus norepinephrine-related dysfunction on tau and its impact on cognition.

This human study tested whether astrocyte reactivity modifies the relationship between locus coeruleus (LC) norepinephrine-related dysfunction, tau pathology, and cognition by combining ultra-high-field LC functional imaging with plasma biomarkers of GFAP and hyperphosphorylated tau (p-tau) and longitudinal cognitive data from 78 asymptomatic individuals. Astrocyte reactivity altered how LC dysfunction related to tau burden and subsequent cognitive decline, indicating an interaction between glial activation and noradrenergic/tau pathways. The findings suggest that astrocyte reactivity is a key modifier of disease-relevant neurobiology in preclinical stages of Alzheimer’s disease.

Prokopiou PC, Van Egroo M, Riphagen JM et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗

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Neuroscience & neural circuit/repair (circuit mapping, neuromodulation, iPSC cell therapy)

Mechanical unloading promotes adult cardiomyocyte proliferation through epicardial NRG1-ERBB4 signaling.

This study tested whether mechanical unloading can restore proliferative capacity in adult cardiomyocytes using heterotopic heart transplantation models in mammals, including infarcted hearts. Mechanical unloading of nonpumping donor hearts induced adult cardiomyocyte proliferation detected by Ki67-based assessment and MADM lineage tracing, and similar unloading in infarcted recipients promoted peri-infarct regeneration. The results implicate epicardial NRG1-ERBB4 signaling as a mechanistic pathway for adult cardiac regeneration, supporting load-reduction strategies combined with ERBB4-targeted approaches.

Jiang C, Liu T, Dai Z et al. · Nature cardiovascular research · (2026) · View on PubMed ↗

Vestibular nucleus stimulation for ameliorating locomotor dynamics in a Parkinsonian mouse model.

This study mapped vestibular nucleus complex (VNC) circuitry in mouse brain and tested whether optogenetic activation of excitatory Vglut2-defined VNC neurons can improve locomotor dynamics in a Parkinsonian mouse model. Optogenetic stimulation at sub-symptomatic intensities increased cFos activity in basal ganglia-associated and brainstem motor hubs and improved locomotor dynamics, consistent with VNC projections to striato-thalamo-subthalamic and caudal medulla motor networks. These findings support vestibular nucleus stimulation as a mechanistically grounded neuromodulation strategy for Parkinson’s axial symptoms that are inadequately treated by medication or deep brain stimulation.

Hartig J, Friedrich MU, Signoret-Genest J et al. · Nature communications · (2026) · View on PubMed ↗

Human spinal interneurons repair the injured rat spinal cord through synaptic integration.

This study engineered human V2a-enriched spinal interneurons from an optogenetic channelrhodopsin-2 (ChR2) expressing human induced pluripotent stem cell (hiPSC) line and assessed their maturation, synaptic connectivity, and functional integration after transplantation into a rat model of cervical spinal cord injury (SCI). Transplanted human V2a interneurons repaired injured circuitry through synaptic integration with host networks, producing functional recovery consistent with circuit-level restoration. The results support a translational strategy using human iPSC-derived interneurons to rebuild synaptic connectivity after SCI.

Zholudeva LV, Agrawal A, Fortino T et al. · Science translational medicine · (2026) · View on PubMed ↗

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Infectious disease & host defense (viral/bacterial/parasitic immunity, vaccines)

Virus reactivation in acute and long COVID-19.

This study analyzed multi-omic longitudinal data from 1,154 hospitalized COVID-19 patients in the IMPACC cohort to characterize temporal dynamics and immunological impact of viral reactivation. It found significant reactivation of Herpesviridae and Anelloviridae during acute COVID-19, with distinct reactivation patterns across viruses and immune states. Clinically, these dynamics suggest that acute SARS-CoV-2 infection can reshape host immunity by triggering reactivation of chronic viruses, with potential implications for complications and risk stratification.

Maguire C, Chen J, Rouphael N et al. · Nature · (2026) · View on PubMed ↗

Multidrug-resistant and virulence traits in genetically distinct vesicular Leptospira inhabiting farmland and sewage in Southern India.

This study isolated six novel environmental Leptospira strains from farmland and sewage in Southern India and characterized their taxonomic identity, multidrug-resistance patterns, and virulence traits using in silico and in vitro assays. Two isolates from sewage near a wildlife enclosure in Mangalore were identified as Leptospira interrogans (SA-L3 and SA-L4), and the work reports strain-specific drug resistance and virulence profiles across genetically distinct Leptospira species. The results highlight locally circulating, genetically diverse, potentially drug-resistant and virulent Leptospira in environmental reservoirs, informing risk assessment and antimicrobial stewardship for leptospirosis.

Sonam A, Hameed A, Stothard P et al. · Scientific reports · (2026) · View on PubMed ↗

Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury.

This study used a DOCA-salt-induced hypertensive mouse model and a primary mouse renal tubular epithelial cell (mTEC)–bone marrow-derived macrophage (BMDM) coculture system to test whether aldosterone-dependent renal injury involves tubular epithelial cell–driven macrophage pyroptosis via PANX1-mediated extracellular ATP (eATP) signaling to P2X7. Aldosterone-dependent injury increased the TEC–macrophage pyroptosis axis, and the study used inhibitors plus AAV-shRNA and siRNA to show that PANX1–eATP–P2X7 signaling is required for macrophage pyroptosis in this context. The results identify a specific molecular crosstalk pathway (PANX1/eATP/P2X7) that could be targeted to reduce inflammatory cell death and fibrosis in aldosterone-driven renal disease.

Wang C, Ma H, Xu J et al. · Cell death & disease · (2026) · View on PubMed ↗

TREM2 plays a critical role in innate immune defense against acute Toxoplasma gondii infection by promoting macrophage antimicrobial activities.

The study assessed the role of the innate immune receptor TREM2 in host defense during acute Toxoplasma gondii infection by comparing TREM2-deficient mice to C57BL/6 wild-type controls after intraperitoneal infection with the type II Prugniaud strain. TREM2 knockout mice showed increased mortality, higher parasite burden, worse liver pathology, and elevated inflammatory cytokines (IL-1α, IL-6, IL-17A) by 7 days post-infection, consistent with impaired macrophage antimicrobial activity. These results position TREM2 as a critical regulator of macrophage effector functions that determine outcome during acute toxoplasmosis.

Debray HZ, Cheng D, Ayala LA et al. · PLoS pathogens · (2026) · View on PubMed ↗

Single amino acid substitution in RdRp reduces viral recombination frequency of NADC30-like porcine reproductive and respiratory syndrome virus type 2.

The study investigated how a single amino acid substitution in the RNA-dependent RNA polymerase (RdRp) affects recombination frequency in NADC30-like porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2). Using serial passaging of two PRRSV-2 strains (NADC30-like HeB108 and HP-PRRSV HuN4) in the presence of ribavirin, the authors identified RdRp changes associated with reduced viral recombination. This links a specific polymerase residue to recombination control, informing how antiviral pressure may alter PRRSV-2 evolutionary dynamics.

Cui X, Song H, Huang X et al. · PLoS pathogens · (2026) · View on PubMed ↗

A structural and mechanistic atlas of NTD antibody neutralization and immune escape across SARS-CoV-2 prototype and its (sub-)variants.

This study mapped neutralizing antibody epitopes and immune-escape mechanisms targeting the SARS-CoV-2 spike N-terminal domain (NTD) across the prototype virus and (sub-)variants by classifying NTD antibodies into nine spatial classes (NTD-1 to NTD-9, including a cryptic NTD-8 epitope). Mechanistic experiments showed that antibodies in classes NTD-5 and NTD-9 neutralize by inducing S1 shedding, and format profiling demonstrated that while most NTD antibodies require bivalency, some (NTD-3, NTD-5, NTD-9) retain neutralization in Fab form. These results provide a structural/functional atlas that can guide design of next-generation NTD-targeting vaccines and therapeutics resilient to immune escape.

Zhou J, Li W, Wang X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Candida albicans activates Staphylococcus aureus virulence regulatory systems to drive toxin-mediated human cell death.

This study tested how Candida albicans co-infection alters Staphylococcus aureus virulence toward host cells, focusing on cytotoxicity mechanisms in murine and human monocytes. C. albicans enhanced S. aureus cytotoxicity in both species, and enhanced killing of murine monocytes required the S. aureus Agr virulence regulatory system and was driven by α-type phenol-soluble modulins and γ-hemolysin. These findings clarify a cross-species regulatory pathway that worsens host cell death during polymicrobial infection and may inform targeted interventions against Agr-dependent toxin production.

Eichelberger KR, Chandrasekaran R, Podar NA et al. · PLoS pathogens · (2026) · View on PubMed ↗

Heterologous prime-boost vaccination against H5 avian influenza: Safety and immunogenicity of a MF59-adjuvanted, cell-culture derived H5N6 vaccine.

This phase 2 extension study evaluated safety and immunogenicity of an MF59-adjuvanted, cell-culture derived H5N6 vaccine (aH5N6c) in adults with different priming histories. Adults primed with MF59-adjuvanted, cell-culture derived H5N1 vaccine (aH5N1c) received either two aH5N6c doses or one aH5N6c plus placebo, while unprimed adults received two aH5N6c doses, and the study measured cross-reactive immune responses and tolerability. The results are important for pandemic preparedness by informing heterologous prime-boost strategies that may broaden antibody responses against H5 viruses.

Van Twuijver E, Versage E, Jacobs RL et al. · Human vaccines & immunotherapeutics · (2026) · View on PubMed ↗

A CEBPB-IPO4-FASN-MAVS axis limits innate immune activation and viral pneumonia.

This study examined how importin β4 (IPO4) and the CCAAT/enhancer-binding protein beta (CEBPB) transcriptional axis regulate antiviral innate immunity in alveolar macrophages, lung ciliated epithelium, and peripheral blood mononuclear cells from patients with severe COVID-19 or influenza, using in vitro and in vivo loss-of-function approaches. IPO4 was downregulated during RNA viral infections via CEBPB-driven transcriptional reduction, and loss of IPO4 increased innate antiviral/inflammatory activation while IPO4 dampened antiviral and inflammatory responses. These findings identify a CEBPB–IPO4–FASN–MAVS regulatory pathway as a potential target to modulate hyperinflammation and viral pneumonia severity.

Wu J, Chen Z, Yin S et al. · Cell reports · (2026) · View on PubMed ↗

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Immunology & immune regulation (autoimmunity, trained immunity, immune cell function)

Antigen presentation by CD40+MHC-II+ astrocytes promotes CNS autoimmunity.

This study tested whether astrocytes can drive CNS autoimmunity by presenting antigen to CD4+ T cells, using rabies barcode interaction detection, single-cell RNA sequencing, in vitro co-cultures, and cell-specific in vivo CRISPR-Cas9 perturbations. Astrocytes expressing CD40 and MHC-II promoted CNS T cell autoimmunity, establishing a functional astrocyte–T cell interaction axis. Demonstrating antigen presentation by CD40+MHC-II+ astrocytes advances mechanistic understanding of autoimmune CNS disease and suggests new immunomodulatory targets beyond conventional immune-cell-centric models.

Lee JH, Li Z, Soto JS et al. · Nature · (2026) · View on PubMed ↗

Peri-weaning, diet-induced activation of an IFNγ-mediated regulatory circuit promotes cDC1 maturation and CD8+ T cell differentiation.

This study investigated how peri-weaning dietary cues shape early-life immunity by defining an IFNγ–STAT1 regulatory circuit in spleen type 1 conventional dendritic cells (cDC1) and its effects on CD8+ T cell differentiation in early-life mice. IFNγ-driven STAT1 signaling induced an immunogenic maturation program in cDC1 that enabled them to direct effector differentiation of antigen-experienced effector memory CD8+ T cells, establishing a dietary-to-IFNγ relay that balances defense and tolerance. The work provides a mechanistic framework for manipulating early-life vaccination or dietary interventions to tune CD8+ T cell outcomes.

Altunöz D, Shakiba R, Ravi Rengarajan K et al. · Nature communications · (2026) · View on PubMed ↗

The deubiquitinase USP4 stabilizes the SCFFBXO24 ubiquitin E3 ligase to regulate immunity in experimental pneumonia.

This study examined how the deubiquitinase USP4 regulates the stability of the SCF^FBXO24 ubiquitin E3 ligase receptor subunit (FBXO24) during experimental Haemophilus influenzae type B (HiB) pneumonia, using THP-1 macrophage cells and in vivo pneumonia models. HiB protected FBXO24 from lysosomal degradation by reducing its ubiquitylation, and USP4 mediated FBXO24 deubiquitylation and stabilization in a TLR4-dependent manner; therapeutic USP4 knockdown via nanoparticle-delivered encapsulated USP4 siRNA (and related approaches) was tested in experimental pneumonia. These findings connect a USP4–FBXO24 stabilization mechanism to innate immune regulation in bacterial pneumonia and suggest a potential host-targeted intervention axis.

Yurtsever I, Farkas D, Cornwell A et al. · Nature communications · (2026) · View on PubMed ↗

TFEB Deficiency Impairs Male Fertility Through Mitochondrial Dysfunction.

The study investigated how transcription factor EB (TFEB) regulates male fertility by using spermatogonia-specific TFEB deletion in mice to model impaired reproductive function. TFEB deficiency caused reduced fertility, impaired sperm motility, decreased androgen production, reduced TNP1 expression (a spermiogenesis marker), and mitochondrial abnormalities in testes and sperm. These findings establish TFEB as a regulator of mitochondrial function required for spermatogenesis and suggest TFEB–mitochondrial pathways as potential targets for male infertility.

Li H, Zhao G, Zong R et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Rate of Autoimmune Diseases in the 10 Years Preceding Myasthenia Gravis Diagnosis: A Nationwide Cohort Study in South Korea.

This nationwide retrospective cohort study in South Korea analyzed Korean National Health Insurance Service claims (2010–2021) to quantify rates and timing of autoimmune diseases in the 10 years before myasthenia gravis (MG) diagnosis. Individuals who later developed MG had distinct temporal patterns and increased rates of other autoimmune diseases in the preceding decade compared with the general population. The results are clinically important for risk prediction and for understanding autoimmune comorbidity trajectories leading up to MG.

Kwon S, Kim BS, Han K et al. · Neurology · (2026) · View on PubMed ↗

Our understanding of the interactions between immune cells and beta cells in the pancreas: autoimmune mechanisms leading to type 1 diabetes.

This expert review synthesized evidence on how immune cells and pancreatic beta cells interact in type 1 diabetes (T1D), focusing on autoimmune mechanisms that begin with beta-cell intrinsic dysfunction. It highlights pathways such as impaired protein processing, endoplasmic reticulum stress, neoantigen formation, and early upregulation of MHC class I that can increase beta-cell immunogenicity and promote autoimmune recognition. The review is significant because it reframes T1D initiation as partly driven by beta-cell biology, informing prevention and therapeutic strategies beyond immune suppression alone.

von Herrath M, Lemos JRN, Krag Knop F · Expert review of clinical immunology · (2026) · View on PubMed ↗

Early versus late JAK-STAT-IFN signaling distinguishes no rejection from subclinical to clinical TCMR after liver transplantation.

This study used longitudinal multimodal immune profiling and single-cell RNA sequencing (scRNA-seq) in 13 adult living-donor liver transplant recipients undergoing an interventional immunosuppression withdrawal trial to distinguish early versus late JAK-STAT-IFN signaling in patients with subclinical TCMR (“nonpermissive”) versus quiescent (“permissive”) allografts at 12 months. Nonpermissive patients showed distinct, biphasic JAK-STAT-IFN immune trajectories compared with permissive grafts despite similar baseline profiles. These findings mechanistically stratify subclinical rejection risk and could guide timing/selection of immunosuppression to prevent progression while enabling safer withdrawal.

Macedo C, Hadjiyannis Y, Tran LM et al. · Science translational medicine · (2026) · View on PubMed ↗

Fecal microbiome transplant in food allergy in humans and mice identifies a role for bile acid metabolites in oral tolerance.

This phase 1 open-label trial (NCT02960074) evaluated oral encapsulated fecal microbiome transplantation (FMT) in 15 adults with peanut allergy and used mouse microbiome transfer to test mechanisms of oral tolerance. FMT increased the peanut reactivity threshold in responders and shifted immune responses toward increased tolerogenic RORγt+ regulatory T cells (Tregs) with decreased TH2 cells, while responder-derived microbiomes protected mice from peanut allergy. The study implicates bile acid metabolites as mediators of microbiome-driven oral tolerance, informing future microbiome- or metabolite-based therapies for food allergy.

Rachid R, Martinez-Blanco M, Kuziel GA et al. · Science translational medicine · (2026) · View on PubMed ↗

BCG HSP70 Reprograms Macrophages via Central Trained Immunity to Suppress Prostate Cancer.

This study investigated whether BCG-derived heat shock protein 70 (BCG HSP70; Dnak) can induce central trained immunity by epigenetic and metabolic reprogramming of bone marrow hematopoietic stem cells and thereby suppress prostate cancer in preclinical models. A single Dnak pretreatment established durable central trained immunity and significantly inhibited tumor growth in prostate cancer models while also conferring protection against bacterial infection. The work supports Dnak as a defined, safer alternative to live BCG for cancer immunotherapy strategies that rely on trained immunity.

Liu P, Liu K, Wang K et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

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Kidney & renal disease mechanisms (DKD, AKI, iron handling, renal injury crosstalk)

Growth Differentiation Factor 15 (GDF15) Protects Against Sepsis-Associated Acute Kidney Injury via Suppression of TLR4-MyD88-NF-κB Signaling and Ferroptosis.

This study examined whether growth differentiation factor 15 (GDF15) protects against sepsis-associated acute kidney injury (SAKI) in human kidney tissue samples and in cecal ligation and puncture (CLP) mice, focusing on TLR4-MyD88-NF-κB signaling and ferroptosis. In CLP mice treated with recombinant GDF15 (rmGDF15, 50 ng/kg i.p.), GDF15 suppressed TLR4-MyD88-NF-κB signaling and ferroptosis, improving renal function (Scr/BUN), kidney injury markers (including KIM-1), inflammatory cytokines (TNF-α/IL-1β/IL-6), and 7-day survival. These findings support GDF15 as a mechanism-based therapeutic candidate for SAKI by targeting upstream innate immune signaling and ferroptotic cell death pathways.

Yang C, Zhao L, Di J et al. · BioFactors (Oxford, England) · (2026) · View on PubMed ↗

Renoprotective effects of tubular glucagon receptor activation mediated by V-ATPase.

The study investigated whether tubular glucagon receptor (GCGR) signaling directly mediates renoprotection in diabetic kidney disease (DKD) using tubule-specific GCGR loss- and gain-of-function mouse models and human kidney samples. Tubular GCGR expression was reduced in DKD and correlated with worse kidney function and greater injury, and genetic ablation of tubular GCGR worsened disease while GCGR gain-of-function improved renal outcomes. These findings identify tubular GCGR as a clinically relevant therapeutic axis for kidney protection, complementing the renal benefits observed with dual GLP-1R/GCGR agonists.

Qu H, Xu M, Du P et al. · Science advances · (2026) · View on PubMed ↗

TPC1-dependent control of endosomal pH and transferrin uptake determines cellular iron status.

This study examined how the endolysosomal two-pore channel TPC1 regulates endosomal pH and transferrin uptake in mice, using a gain-of-function TPC1I486T mutation and TPC1 knockout models. Patch-clamp experiments showed that TPC1I486T markedly increased TPC1 channel activity upon early endosome activation by endogenous phosphatidylinositol 3-phosphate, shifting endosomal pH/transferrin uptake to drive iron overload (while TPC1 loss caused iron deficiency). These findings identify TPC1 as a mechanistic control point for cellular iron status and suggest that TPC1 modulation could be relevant for iron-overload disease strategies.

Deutsch R, Jörs S, Klingl Y et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

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Genetics & inherited disease architecture (monogenic/oligogenic, rare variants)

Oligogenic inheritance in epilepsy: A systematic exome-wide analysis.

This systematic exome-wide analysis evaluated monogenic versus oligogenic inheritance in epilepsy using exome data from 422 patients with epilepsy and 5308 nonepileptic controls from the Epi25 Collaborative project. The study assessed the burden and contribution of deleterious variants across epilepsy genes under models allowing incomplete penetrance and variable expressivity, consistent with an oligogenic contribution to disease risk. Clinically, the results support a more nuanced genetic architecture for epilepsy that may improve variant interpretation and risk prediction beyond single-gene explanations.

Duerinckx S, Gravel B, Soblet J et al. · Epilepsia · (2026) · View on PubMed ↗

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Developmental biology & regeneration (tissue regeneration, growth, fertility, autophagy programs)

Maternal hyperglycemia-induced O-GlcNAcylation of CaMKIIδ promotes mtDNA release and cardiac remodeling in offspring.

This study used an intrauterine hyperglycemia rodent model to examine how maternal gestational diabetes affects neonatal cardiac remodeling, focusing on O-GlcNAcylation of CaMKIIδ and downstream mitochondrial DNA (mtDNA) release. Offspring exposed to gestational diabetes showed increased O-GlcNAcylation in neonatal hearts, along with mtDNA release, cardiac remodeling, and inflammatory responses, with mechanistic support from RNA sequencing and mitochondrial functional analyses. These findings identify a CaMKIIδ O-GlcNAcylation–mtDNA axis as a potential therapeutic target to prevent diabetes-associated congenital or early-life cardiac dysfunction.

Xiao Z, Gao L, Wang Y et al. · Nature communications · (2026) · View on PubMed ↗

Human growth plates house resting zone sub-populations with features of quiescent stem cells.

This study applied spatially resolved transcriptomics to human growth plate biopsies from healthy adolescents undergoing epiphysiodesis for idiopathic tall stature to define transcriptional networks and zone-specific sub-populations. It identified resting-zone sub-populations with features of quiescent stem cells and discovered a novel hypertrophic zone marker, SGMS2, which was found in growth plate-derived matrix vesicles and whose activity promoted mineralization. These findings improve the molecular atlas of human growth plate biology and point to SGMS2 as a candidate regulator relevant to growth disorders involving impaired mineralization.

Avijgan M, López-Pérez AR, Galicia LA et al. · Bone research · (2026) · View on PubMed ↗

IGSF10 regulates osteogenesis and osteoclastogenesis via a noncanonical EGFR-STAT1 signaling axis to promote skeletal regeneration.

This study identified IGSF10 as a dual regulator of bone remodeling and tested its role in osteogenesis and osteoclastogenesis using Igsf10-deficient mice and knockout cell assays, alongside recombinant IGSF10 protein rescue experiments. Igsf10 deficiency caused reduced bone mass with elevated osteoclast activity and impaired osteogenesis, while recombinant IGSF10 restored osteogenic capacity and suppressed osteoclastogenesis, acting through a noncanonical EGFR–STAT1 signaling axis. These results position IGSF10 and its EGFR–STAT1 pathway as potential therapeutic targets to coordinate bone formation and resorption during skeletal regeneration.

Wen J, Deng Y, Jiang R et al. · Bone research · (2026) · View on PubMed ↗

A transposon-derived transcription factor senses ionic stress through phase separation to govern plant autophagy.

The study investigated how a transposon-derived transcription factor, MUSTANG4 (MUG4), senses ionic stress via phase separation to regulate plant autophagy. Under salt/ionic stress conditions, MUG4 formed phase-separated assemblies that enabled ionic-stress perception and promoted autophagy gene regulation, providing a plant-specific master control mechanism analogous to TFEB-driven autophagy programs in animals. This advances understanding of how plants translate ionic stress signals into transcriptional programs that enhance stress tolerance.

Shao Y, Wang S, Liang L et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Unveiling previously undescribed circadian clock regulators and action mechanisms via TurboID-based profiling of the LWD1 interactome in Arabidopsis thaliana.

The study used TurboID-based proximity labeling to map the LWD1 interactome at three Zeitgeber times (ZT) in Arabidopsis thaliana to uncover previously undescribed circadian clock regulators and action mechanisms. It identified 219 LWD1-interacting proteins across time points and experimentally validated selected partners as new regulators of circadian outputs. This expands the molecular network controlling plant circadian timing and provides candidate components for dissecting how LWD1 coordinates clock gene expression.

Huang CK, Hsu CC, Tsai HL et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

An N-acetylated daropeptide modulates nematode development.

This study investigated the natural product aphotorhaptin A, an N-acetylated daropeptide (daropeptide) from the symbiotic bacterium Photorhabdus asymbiotica, and how its biosynthesis and maturation affect nematode development. Biosynthetic analyses indicated aphotorhaptin A is processed by an unexpected leader cleavage step and that N-terminal acetylation increases metabolic stability while preserving the hexapeptide scaffold. The work expands understanding of ribosomally derived daropeptide maturation and highlights N-terminal acetylation as a key feature for bioactivity in host–symbiont interactions.

Ma S, Li R, Gao X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

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Epigenetics, chromatin & RNA regulation (TF access, m7G, lactylation, P-bodies, translation control)

A molecular switch for coordinating kinesin and dynein transport of mitochondrial cargo.

A regulatory helix in the mitochondrial adaptor protein TRAK (trafficking kinesin-binding protein) was studied to explain how cells switch mitochondrial transport between kinesin and dynein. Using a synthetic cargo transport assay and AlphaFold2-guided mutagenesis, the authors identified a helix sequence in TRAK that coordinates the kinesin–dynein transport switch, and showed that two near-identical TRAK isoforms drive different transport behaviors. This provides a mechanistic molecular switch for bidirectional mitochondrial trafficking, informing how cells dynamically redistribute mitochondria under stress.

Gladkova C, Paez-Segala MG, Grant WP et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

An ancient mitochondrial program tunes translation to haem availability.

This study explored how an ancient mitochondrial program regulates translation in response to haem availability, focusing on the cellular circuitry that senses haem levels. The work identifies a mitochondrial translational control mechanism that tunes protein synthesis according to haem availability, coordinating haem homeostasis during erythroid differentiation and stress conditions such as iron deficiency or thalassemia. By clarifying how haem is monitored to balance essential function and toxicity, the findings advance mechanistic understanding of anaemia biology and potential targets for disorders of haemoglobin imbalance.

Zhang X, Schuler MH, Çetin G et al. · Nature · (2026) · View on PubMed ↗

Bruno 1 remodels P-bodies to protect select mRNAs during the early ER stress response.

This study investigated how the RNA-binding protein Bruno 1 (Drosophila melanogaster) remodels P-bodies during the early response to endoplasmic reticulum (ER) stress in oogenesis, upstream of stress granule formation. Bruno 1 was transcriptionally upregulated downstream of ATF4-dependent stress signaling and drove rapid (minutes) P-body morphological/organizational remodeling that promoted selective mRNA storage. The work identifies an ATF4→Bruno 1→P-body remodeling axis as a conserved strategy for managing mRNA fate during ER stress, with implications for how cells preserve specific transcripts under proteostasis stress.

Milano SN, Bayer LV, Ko JJ et al. · Life science alliance · (2026) · View on PubMed ↗

Skeletal muscle H3K18 lactylation inhibits hepatic gluconeogenesis through IL-6 mediated interorgan communication.

This study investigated how skeletal muscle lactate signaling regulates hepatic glucose production in type 2 diabetes by focusing on H3K18 lactylation and IL-6–mediated interorgan communication, using mouse models with skeletal muscle-specific Ldha (LDHA) ablation and human correlation analyses. Elevated circulating lactate derived from skeletal muscle with high Ldha expression correlated with hyperglycemia, and disrupting Ldha in skeletal muscle impaired whole-body glucose homeostasis via increased hepatic gluconeogenesis driven by IL-6 signaling. These findings identify a skeletal muscle epigenetic modification axis (H3K18 lactylation) coupled to IL-6 as a potential therapeutic target to improve glucose control in type 2 diabetes.

Wang Y, Wang F, Sun Y et al. · Science advances · (2026) · View on PubMed ↗

Cohesin facilitates nucleosome invasion by transcription factors.

The study examined how cohesin influences transcription factor (TF) access to nucleosomal DNA, using the bacterial TF LexA ectopically expressed in yeast. LexA, despite poor nucleosome binding in vitro, rapidly invaded a well-positioned nucleosome in vivo when its motif was positioned at the dyad, suggesting TFs can exploit nucleosome dynamics rather than relying solely on static binding affinity. This provides a mechanistic framework for how chromatin remodelers like cohesin may facilitate pioneer-factor-like nucleosome invasion and thereby regulate gene expression programs.

Stoeber S, Chen H, Chen RW et al. · Science advances · (2026) · View on PubMed ↗

Molecular determinants of functional voltage-gated sodium (Nav) channel diversity in mammalian central neurons.

The study reviewed and analyzed molecular determinants that generate diversity among voltage-gated sodium (Nav) channel currents in mammalian central neurons, focusing on transient (INaT), persistent (INaP), and resurgent (INaR) components. It synthesized how differences in Nav channel subunit expression and biophysical properties shape neuronal firing patterns and circuit-level behaviors. This is significant for understanding how channel diversity contributes to excitability, plasticity, and homeostasis, with implications for interpreting and targeting neurological disorders.

Ransdell JL, Nerbonne JM · The Journal of physiology · (2026) · View on PubMed ↗

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Bioengineering & computational biology (AI models, spatial proteomics foundation models, cfDNA ML)

Generative design of bacteriophages with genome language models.

Generative genome language models were used to design complete bacteriophage genomes, with experimental validation using phage ΦX174 as a template and testing for host tropism and fitness. The approach generated viable phages with diverse fitness profiles, and cryo-electron microscopy showed that a generated phage used an evolutionarily distant DNA packaging protein in its capsid. This demonstrates an AI-guided route to engineer phages with tailored properties, including cocktails that can overcome ΦX174-resistant E. coli strains.

King SH, Driscoll CL, Li DB et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

The Virtual Tissues foundation model resolves spatial proteomics across scales.

This study developed and evaluated Virtual Tissues (VirTues), a foundation model for spatial proteomics that learns multi-scale representations from multiplex imaging data. VirTues enables marker-aware protein reconstruction, cell segmentation and typing, and niche annotation across spatial proteomics datasets, improving cross-cohort knowledge transfer for robust biomarker discovery. A general-purpose, pretrained spatial proteomics model can accelerate translational cancer research by standardizing analysis across heterogeneous marker panels and experimental protocols.

Wenckstern J, Jain E, von Querfurth B et al. · Nature · (2026) · View on PubMed ↗

Integrative cfDNA profiling from low-pass whole-genome sequencing enables tissue-of-origin prediction in cancer.

This study developed an integrative circulating cell-free DNA (cfDNA) profiling approach using low-pass whole-genome sequencing and a stacked ensemble machine learning classifier to predict tissue of origin (TOO) in cancer, including cancers of unknown primary (CUP) and multiple primary cancers (MPC). By integrating 11 cfDNA feature types spanning genomic, fragmentomic, methylation/repeat, and microbial signals, the model achieved improved TOO prediction performance under five-fold cross-validation. This provides a clinically actionable framework for noninvasive TOO inference from cfDNA to guide diagnosis and treatment selection in heterogeneous cancers.

Zhang Y, Liu L, Bao H et al. · Molecular biomedicine · (2026) · View on PubMed ↗

Sharp nanothorn-equipped ionogel microrobots for targeted periodontitis therapy.

This study engineered sharp nanothorn-equipped magnetically actuated ionogel microrobots loaded with curcumin to overcome periodontal barriers and treat periodontitis. The microrobots used gold nanothorns to disrupt biofilms and penetrate mucus, enabling targeted antibacterial delivery under magnetic navigation in viscous environments. The approach suggests a platform technology for locally effective, barrier-penetrating therapy in periodontitis where conventional drug delivery is limited.

He D, Zou Z, Jin D et al. · Science advances · (2026) · View on PubMed ↗

Leveraging IGF signaling to improve the spatial organization and regenerative potential of iPSC-derived vascularized liver organoids.

This study created vascularized liver organoids by combining human iPSC-derived hepatoblasts and endothelial cells in decellularized scaffolds functionalized with an anti-CD31 aptamer-based vascular coating agent (VCA), then used spatial transcriptomics and perturbation to identify signaling drivers. The organoids achieved spatially coordinated organization of vasculature and parenchyma, and perturbation implicated the IGF2–IGF1R–AKT/MAPK signaling axis as a key regulator of spatial organization and functional maturation. These results advance iPSC-based liver tissue engineering by defining a growth-factor pathway to improve vascular patterning and regenerative performance.

Kim DH, Lee Y, Kim MJ et al. · Science advances · (2026) · View on PubMed ↗

3D epigenomic landscape of the human retinal pigment epithelium.

This study integrated multi-omics data to benchmark the 3D epigenomic landscapes of primary human retinal pigment epithelium (hRPE), induced pluripotent stem cell–derived RPE (iPSC-RPE), and the ARPE-19 cell line. The analysis found that iPSC-RPE adopts a mixed molecular state and only partially recapitulates the epigenomic features of primary hRPE compared with ARPE-19. The work is significant for improving iPSC-RPE engineering and for understanding why functional visual gains in cell replacement therapies have been modest.

Liu X, Tang D, Zhang J et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

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Clinical trials, guidelines, and health economics (real-world studies, codes of conduct, cost-effectiveness, trials)

Lecanemab use in Chinese patients with Alzheimer’s disease: a 12-month multicenter real-world study.

Lecanemab was evaluated in a real-world, 12-month multicenter cohort of 1,042 Chinese patients with Alzheimer’s disease, with outcomes including ARIA, infusion-related reactions, and cognitive change measured by CDR-SB. ARIA occurred in 7.87% and infusion-related reactions in 16.12%, and the study assessed CDR-SB score change over follow-up timepoints. These data support the safety profile and potential cognitive utility of lecanemab in routine clinical practice in Chinese patients, including the role of blood-based biomarkers for treatment guidance.

Wu H, Chen Q, Fang M et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗

Anti-TNF withdrawal or long-term treatment in ulcerative colitis (BIOSTOP): a multicentre open label, randomized controlled trial.

In the BIOSTOP randomized controlled trial, anti-TNF withdrawal versus continued long-term anti-TNF maintenance was studied in ulcerative colitis patients who were in deep clinical, biochemical, and endoscopic remission. The trial compared endoscopically confirmed remission (Mayo Endoscopic Score 0 or 1) after two years, allowing flares to be treated with anti-TNF or non-biologic agents. Results will clarify whether stopping anti-TNF is non-inferior to maintenance, informing duration-of-therapy decisions to balance efficacy and treatment burden in UC.

Berset IP, Lerang F, Moum B et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

Tirzepatide and the risk of atherosclerotic cardiovascular events: population based cohort study.

This population-based cohort study used two US claims databases (May 2022 to May 2025) to compare tirzepatide versus sitagliptin in 52,971 adults aged ≥40 years with type 2 diabetes and established atherosclerotic cardiovascular disease. The key finding was an estimated reduction in major adverse cardiovascular events (MACE) with tirzepatide added to standard of care compared with the cardiovascular-outcome-neutral comparator. If confirmed, these real-world results support tirzepatide as a potentially beneficial therapy for reducing cardiovascular events in high-risk patients with diabetes.

Krüger N, Schneeweiss S, Wang SV · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

Gynecologic Cancer InterGroup code of conduct for diversity in gynecological cancer trials: a clinical guide from the Berlin Gynecologic Cancer InterGroup meeting.

This article presents a clinical guide/code of conduct developed by the Berlin Gynecologic Cancer InterGroup to improve diversity and representation across gynecologic cancer trials. The key output is a structured, practice-oriented Code of Conduct adopted by 33 member groups that translates diversity principles into actionable steps across all phases of clinical research. Scientifically and clinically, it aims to increase generalizability and equity of evidence for under-represented populations in gynecologic oncology.

Sehouli J, Bookman MA, Harter P et al. · International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · (2026) · View on PubMed ↗

Omission of axillary lymph node dissection in ultrasound-detectable axillary metastases in primary breast cancer treated by upfront surgery: prospective randomized SENOMAC-ULTRA non-inferiority trial.

This prospective randomized SENOMAC-ULTRA non-inferiority trial evaluated whether targeted axillary dissection (TAD) can safely replace axillary lymph node dissection (ALND) in patients with clinically node-positive primary breast cancer undergoing upfront surgery. The trial’s design compares ALND versus TAD to reduce arm morbidity while maintaining oncologic safety in a clinically node-positive population where omission of ALND is not standard. If successful, the study could change surgical management by expanding less invasive axillary approaches beyond sentinel-node–limited disease.

de Boniface J, Meretoja T, Rydén L et al. · BJS open · (2026) · View on PubMed ↗

The role of ceramides in the pathophysiology of diabetic retinopathy: Mechanisms and Implications for therapeutic strategies.

This review examined the role of ceramides—bioactive sphingolipids—in diabetic retinopathy (DR) pathophysiology and how they contribute to apoptosis, inflammation, and oxidative stress. It concludes that ceramide accumulation can exacerbate retinal neurodegeneration by modulating key molecular pathways and summarizes emerging therapeutic strategies aimed at targeting ceramide biology. The synthesis supports ceramide-centered mechanisms as potential drug targets to slow or prevent DR progression.

Niu X, Huang Y, Sun C et al. · Diabetes & vascular disease research · (2026) · View on PubMed ↗

Xiao-Chai-Hu-Tang alleviates irinotecan-induced diarrhea via promoting bile acid reabsorption and decreasing focal adhesion kinase signaling revealed by metabolomics and proteomics.

The study evaluated Xiao-Chai-Hu-Tang (XCHT) for its ability to treat irinotecan (CPT-11)-induced diarrhea in mice and used integrated metabolomics and proteomics to define mechanisms. XCHT improved CPT-11–associated diarrhea and promoted bile acid reabsorption while decreasing focal adhesion kinase (FAK) signaling. This provides a mechanistic basis for XCHT’s supportive care effect in chemotherapy-induced diarrhea and identifies bile acid handling and FAK signaling as actionable pathways.

He Z, Chen Y, Qiu H et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Syncope.

This article reviewed the clinical evaluation and management of syncope, focusing on reflex, orthostatic, and cardiac mechanisms in patients presenting with transient cerebral hypoperfusion. It emphasizes that accurate diagnosis depends on history, physical examination, and targeted testing guided by risk stratification, with management aimed at preventing recurrence and injury. The review is clinically significant because it outlines practical, mechanism-based approaches to identify high-risk features early, especially in older adults with falls.

Kenny RA · The New England journal of medicine · (2026) · View on PubMed ↗

Eligibility for Anti-Amyloid Therapies in Patients With Biomarker-Confirmed Atypical Alzheimer Disease Phenotypes.

The study assessed whether published eligibility criteria for anti-amyloid therapies (AATs) apply to atypical Alzheimer disease (AD) phenotypes by performing a retrospective eligibility analysis of patients evaluated at the Mayo Clinic. It tested theoretical trial eligibility for posterior cortical atrophy (PCA), logopenic variant primary progressive aphasia (lvPPA), dysexecutive AD (dAD), and corticobasal syndrome because of AD (CBS-AD) using landmark inclusion/exclusion criteria. This is significant for guiding real-world treatment decisions and for designing future trials that include atypical AD presentations.

Shir D, Corriveau-Lecavalier N, Jones DT et al. · Neurology · (2026) · View on PubMed ↗

Dynamic prediction of HIV-related incomplete immune reconstitution: A multicenter, large cohort study using advanced joint modeling.

This multicenter cohort study developed a dynamic joint prediction system for incomplete immune reconstitution (DJPSIIR) using Bayesian joint modeling in 21,862 people living with HIV (PLWH) across 31 Chinese provinces (2003–2024). By integrating longitudinal CD4+ T cell counts and CD4/CD8 ratios with clinical parameters, DJPSIIR produced real-time risk estimates and showed strong discriminatory performance for predicting IIR. The model enables dynamic, individualized monitoring beyond single-time-point risk scores, potentially improving timing of interventions to reduce morbidity and mortality from IIR.

Liu F, Zhang H, Wang X et al. · Science advances · (2026) · View on PubMed ↗

Weight Loss-Dependent Changes in Body Composition and Bone Health in People With Obesity and Type 1 Diabetes Treated With Liraglutide, Semaglutide, or Tirzepatide.

This real-world observational study evaluated 12-month changes in body composition and bone health in people with obesity and type 1 diabetes treated with GLP-1 receptor agonists (liraglutide or semaglutide) or the dual GIP/GLP-1 receptor agonist tirzepatide. Using DEXA to measure regional/total fat and lean mass and bone mineral density (BMD)/bone mineral content (BMC), the study assessed overall changes and stratified outcomes by percentage weight loss. The results are clinically relevant for balancing cardiometabolic benefits of incretin-based therapies with potential effects on skeletal health in T1D patients.

Al Ozairi E, Irshad M, Alkandri J et al. · Diabetes/metabolism research and reviews · (2026) · View on PubMed ↗

Comparative Analysis of Safety Profiles of Pulsed Field and Thermal Energy Atrial Fibrillation Ablation: Insight From the Multicenter Real-World Ablation Registry.

This multicenter real-world registry study compared acute procedural outcomes and safety between pulsed-field ablation (PFA) and thermal ablation for atrial fibrillation in Japan. Among 4,969 index AF ablations (Jan 2024–Jul 2025), PFA and thermal approaches were evaluated for differences in sedation depth and safety endpoints, with PFA performed more often under deep sedation. The findings help inform comparative safety considerations for adopting large-footprint PFA systems in routine AF ablation practice.

Inaba O, Miyazaki S, Nitta J et al. · Journal of cardiovascular electrophysiology · (2026) · View on PubMed ↗

Atopic Dermatitis Flare Following Initiation of Nemolizumab.

This case report described a 49-year-old male with treatment-resistant atopic dermatitis who developed a dyshidrotic-eczema–like vesiculobullous eruption after starting nemolizumab, an IL-31 inhibitor. Within weeks of initiation, he developed new palm-localized pruritic vesiculobullous lesions while pre-existing AD lesions remained stable. The report highlights a potential paradoxical or adverse inflammatory skin reaction associated with nemolizumab initiation that warrants clinician awareness and monitoring.

Burke OM, Beer J, Elman SA · Journal of drugs in dermatology : JDD · (2026) · View on PubMed ↗

Speed of Response in Biologic Treatments for Moderate-to-Severe Plaque Psoriasis: Bayesian Network Meta-Analysis.

This Bayesian network meta-analysis compared the speed of early response (first 8 weeks) among biologics for moderate-to-severe plaque psoriasis, using data from 53 phase 2b/3 randomized controlled trials. It synthesized efficacy outcomes (PASI 75/90/100) for IL-17 inhibitors, IL-23 inhibitors, and TNF-α inhibitors to estimate which therapies achieve faster and greater early improvements. The findings can inform treatment selection by prioritizing rapid disease control in addition to overall efficacy.

Shami MZ, Amara S, Shimon SV et al. · Journal of drugs in dermatology : JDD · (2026) · View on PubMed ↗

Approved Monoclonal Antibody Therapies for Hidradenitis Suppurativa.

This economic evaluation assessed the efficiency frontier of approved monoclonal antibody therapies for hidradenitis suppurativa (HS) across multiple countries by combining phase 3 trial efficacy data for adalimumab, secukinumab, and bimekizumab with drug pricing data. Using publicly available clinical trial results and pricing as of January 31, 2026, the analysis compared cost-effectiveness/efficiency across settings in the US, Canada, France, Germany, and Australia. The study provides payer- and health-system-relevant comparative value information to guide HS biologic selection under budget constraints.

Pham J, Sholji T, Aghajani M et al. · JAMA dermatology · (2026) · View on PubMed ↗

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Generated automatically on August 07, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.