PubMed Trending Research Digest — May 27, 2026

Automated digest · 96 articles · 15 research areas · May 27, 2026

Overview

Across this week’s papers, a dominant theme is immune modulation—both in cancer and in inflammatory disease—by targeting specific upstream regulators of immune dysfunction. In hepatocellular carcinoma, genetic and mechanistic work points to CR1 and PGK1-driven macrophage programs that reshape the immunosuppressive niche and blunt CD8+ T-cell activity, while multiple studies in cancer emphasize how tumor microenvironment states (macrophage suppression, TAM dysfunction, and spatially mapped gene perturbations) can be converted into actionable vulnerabilities. Complementing these, several mechanistic immune studies connect mitochondrial danger signals (e.g., mitoFLARE dysfunction triggering STING in sepsis) and macrophage metabolic reprogramming (GPR161→C5aR1→glycolysis in ARDS) to inflammatory outcomes—reinforcing a broader “immunity is metabolically and organelle-controlled” message.

A second major thread is mitochondria-centered biology as a lever for disease modification. Multiple neurodegeneration papers highlight mitochondrial quality control and intercellular mitochondrial transfer (CHCHD2/CHCHD10 autophagy, irisin-driven α-syn clearance via microglial phagocytosis, and GPNMB/mitochondrial EV transfer in tauopathy), while oncology studies use mitochondrial redox and energy pathways to govern ferroptosis and therapy response (SLC25A13/STAT3 in TNBC; HDAC4 as a SUMO ligase controlling ferroptosis and radiation sensitivity). Even outside these domains, mitochondrial metabolism appears in cardiometabolic and systemic contexts (e.g., dehydration-driven lipid synthesis; copper depletion impairing mitochondrial complex IV in CNS leukemia), suggesting mitochondria remain a unifying target across organ systems.

Finally, the digest shows a strong push toward better prediction and better tools: large-scale biomarker genetics (rare exome variants for lipids; Lp(a) risk stratification and PCSK9-base editing), improved clinical trial design/endpoint thinking (PBC Delphi consensus; pregnancy safety comparisons in IBD; sham-controlled ablation), and increasingly sophisticated experimental and computational platforms (spatial CRISPR mapping, explainable multi-omics models, standardized α-synuclein overexpression constructs, and cryo-EM/FIB-SIMS chemical mapping). Together, these studies reflect a field moving from single-mechanism insights toward integrated, targetable pathways paired with translationally relevant measurement strategies.

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Cancer immunotherapy & tumor microenvironment

Uncovering spatially resolved functional genomics with CRISPR screen sequencing.

This study developed spatial CRISPR screen sequencing (SPAC-seq) and a statistical toolkit (TARDIS) to link gene perturbations to spatial phenotypes and signaling pathways in tissues. Using SPAC-seq/TARDIS, it found that Icam1 loss in tumor cells promotes metastasis through immune suppression and macrophage polarization, and it further implicated Cd44 in CD8+ T cell biology. The work is significant because it provides a high-throughput, spatially resolved functional genomics framework to identify actionable gene–pathway mechanisms in cancer microenvironments.

Zhang H, Zhang Z, Wang P et al. · Cell · (2026) · View on PubMed ↗

Mutational Landscape and Treatment Response in Extensive-Stage Small-Cell Lung Cancer: A Single-Center Real-World Analysis.

This single-center real-world analysis studied the mutational landscape and treatment response in extensive-stage small-cell lung cancer (ES-SCLC), comparing chemoimmunotherapy (CIT) versus chemotherapy (CT) alone. It analyzed 170 ES-SCLC patients treated between 2020 and 2024 and assessed how gene mutation characteristics relate to clinical indicators and subgroup treatment responses. The study is significant because it provides real-world evidence on how genomic features may influence CIT versus CT effectiveness in a “cold” immune-profile cancer subtype.

Li M, Guo L, Zhao R et al. · Current oncology (Toronto, Ont.) · (2026) · View on PubMed ↗

CR1(+) tumor-associated macrophages orchestrate an immunosuppressive niche in hepatocellular carcinoma: a genetic and multi-omics dissection.

This study investigated complement receptor 1 (CR1) as an upstream genetic regulator of tumor-associated macrophage (TAM) dysfunction and immunosuppressive niche formation in hepatocellular carcinoma (HCC) using Mendelian randomization and multi-omics profiling. Integrating MR/metabolite mediation with bulk, single-cell, and spatial transcriptomics, the authors identified CR1-associated programs that orchestrate an immunosuppressive TAM niche in HCC. The work provides a genetic and mechanistic rationale for targeting CR1-regulated macrophage pathways to improve immunotherapy responsiveness in HCC.

Wang Z, Wang Z, Ji X et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Long-term follow-up results of anti-BCMA CAR-T cell therapy combined with autologous hematopoietic stem cell transplantation in relapsed/refractory multiple myeloma with extramedullary disease.

This clinical study evaluated long-term outcomes of anti-BCMA CAR-T cell therapy combined with autologous hematopoietic stem cell transplantation (auto-HSCT) in relapsed/refractory multiple myeloma (R/R MM) with extramedullary disease (EMD). Among 18 enrolled patients, eight received the combination with auto-ASCT (T-C group), and the study reports follow-up efficacy and durability of this combined approach. The significance is that it informs whether adding auto-HSCT to anti-BCMA CAR-T can improve long-term control in a high-risk EMD subset of R/R MM.

Li X, Liu C, Niu S et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Transcriptional states define dependencies and therapeutic vulnerabilities in head and neck cancer.

This work studied how transcriptomic states in head and neck squamous cell carcinoma (HNSCC)—separately for HPV-negative disease—can be mapped to mechanistic survival circuits and drug-actionable therapeutic vulnerabilities. By integrating multi-cohort RNA-seq from 727 tumors with genome-scale CRISPR dependency maps and pharmacologic screening, the authors defined distinct survival circuits including a proliferative axis involving MYC and MET/FAK and nominated subtype-matched therapeutic strategies. The approach provides a mechanistic, decision-oriented framework to translate RNA heterogeneity into targeted treatment selection for HNSCC.

Vaz JM, Zhu S, Useche M et al. · NPJ precision oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomized, multiarm, run-in phase trial.

This run-in phase trial studied whether the vitamin D receptor (VDR) agonist paricalcitol can be safely combined with first-line gemcitabine plus albumin-bound paclitaxel (GA) in 36 patients with metastatic pancreatic cancer, using pretreatment and on-treatment tumor biopsies for pharmacodynamic analyses. Paricalcitol was reported to be safely administered with GA, with oral dosing showing a high proportion of patients experiencing an adverse event signal (5 patients, 42%, receiving oral paricalcitol—text truncated). If confirmed in the full trial, adding paricalcitol to GA could provide a clinically actionable strategy to modulate the tumor microenvironment (including cancer-associated fibroblast quiescence) to improve chemotherapy efficacy in metastatic pancreatic cancer.

Perez KJ, Dias Costa A, Jordan A et al. · Nature cancer · (2026) · View on PubMed ↗

Durvalumab plus anlotinib versus durvalumab alone as maintenance treatment in extensive-stage small-cell lung cancer (DURABLE): a multicenter, randomized, phase II trial and biomarker analysis.

This multicenter, open-label randomized phase II trial (DURABLE; NCT04985851) studied whether durvalumab plus anlotinib improves outcomes versus durvalumab alone as consolidative maintenance therapy in 66 patients with extensive-stage small-cell lung cancer (ES-SCLC) after first-line durvalumab plus platinum–etoposide. The primary endpoint was blinded independent central review-assessed progression-free survival (PFS) from randomization, with a two-sided p-value <0.20 considered statistically significant, but the abstract is truncated before reporting the efficacy results. If durvalumab–anlotinib improves PFS and safety, it could establish a new maintenance regimen for ES-SCLC and inform biomarker-driven patient selection.

Zhang B, Zhong R, Shi C et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Explainable machine learning-guided integrated multiomics analysis reveals macrophage-driven immune suppression in breast cancer.

This study developed an explainable machine learning (XML) pipeline to integrate multiomics features of the breast tumor microenvironment (TME) and relate macrophage-driven immune suppression to relapse-free survival (RFS) and response outcomes. Applying the pipeline to estimated cell fractions from METABRIC and TCGA, and comparing associations with relapse-free survival and pathological complete response (pCR) after neoadjuvant chemotherapy (NAC), the authors concluded that macrophage-associated immune suppression is linked to worse outcomes (details truncated). The significance is that explainable, multi-dataset modeling can nominate actionable TME targets—specifically macrophage-driven suppression—for improving breast cancer prognosis and therapy response.

Azimzade Y, Haugen MH, Kristensen VN et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Pembrolizumab plus high-dose IL-2 in advanced clear cell renal cell carcinoma: six-year survival outcomes and molecular signatures from a phase 2 trial.

This phase 2 clinical study evaluated a fixed-duration regimen of pembrolizumab plus high-dose interleukin-2 in treatment-naive advanced clear cell renal cell carcinoma (ccRCC) and reported long-term outcomes and molecular signatures from trial NCT02964078. With a median follow-up of 76.4 months, the regimen met its prespecified safety/response objectives earlier and the long-term analysis provided extended overall response and progression-free survival/treatment-free interval data along with molecular correlates of response (details truncated in the abstract). Clinically, the work supports the durability of benefit from this chemo-free immunotherapy combination and helps identify biomarkers that may guide patient selection in advanced ccRCC.

Johnson JS, Miller JW, Hatoum F et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Autologous macrophage therapy increases transplant-free survival in cirrhosis: Long-term follow-up of a phase 2 clinical trial.

This phase 1/2 MATCH01 trial and its long-term follow-up study evaluated autologous monocyte-derived macrophage therapy in participants with liver cirrhosis. Macrophage-treated patients showed significantly improved transplant-free survival over extended follow-up (up to ~4 years from randomization). These results support macrophage-based regenerative/anti-inflammatory therapy as a potentially durable, transplant-sparing approach for cirrhosis.

Brennan PN, Kilpatrick AM, Glover A et al. · Cell stem cell · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of bispecific T-cell engagers after CAR T-cell therapy failure in aggressive large B-cell lymphoma.

A systematic review and meta-analysis evaluated bispecific T-cell engagers (BiTEs) in patients with aggressive large B-cell lymphoma who relapsed or progressed after CAR T-cell therapy failure. Across included studies, pooled overall response rate was 51% with pooled complete remission rate of 31%, with pooled progression-free survival of 31% and overall survival of 48%. These findings support BiTEs as an evidence-based post–CAR T option and help quantify expected efficacy in this high-unmet-need setting.

Kharfan-Dabaja MA, Reljic T, Abdel-Razeq S et al. · Current research in translational medicine · (2026) · View on PubMed ↗

PGK1 Suppresses CD8+ T Cell-Mediated Antitumor Immunity Through CCL2/CCR2/Tumor-Associated Macrophages Axis in Hepatocellular Carcinoma.

This mechanistic study in hepatocellular carcinoma (HCC) investigated how phosphoglycerate kinase 1 (PGK1) suppresses CD8+ T cell-mediated antitumor immunity through the CCL2/CCR2 axis involving tumor-associated macrophages (TAMs). It showed that tumor cell–intrinsic PGK1 promotes tumor progression by inhibiting CD8+ T cell antitumor activity and that TAMs are key mediators of this immunosuppressive pathway. These results identify the PGK1–CCL2/CCR2–TAM axis as a potential therapeutic target to enhance immune checkpoint inhibitor responsiveness in HCC.

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

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Cancer cell-intrinsic survival, metabolism & stress responses

Genome-Wide CRISPR Screen Identifies a microRNA Orchestrating Pleiotropic Resistance to Targeted Therapy and T Cell Immunity in Melanoma.

This study used a genome-wide microRNA (miRNA) CRISPR knockout screen integrated with cellular models, longitudinal clinical samples, and in vivo experiments to identify miRNAs driving pleiotropic resistance in melanoma. It identified miR-18a as a pivotal upstream regulator of cross-resistance to targeted therapy and CD8+ T cell-mediated cytotoxicity, showing that miR-18a loss confers resistance via derepression of AJUBA-regulated pathways (and additional mechanisms). The work is significant because it links a specific miRNA to combined therapy resistance and immune evasion, suggesting miR-18a as a candidate target to improve melanoma treatment responses.

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

A sweet danger: the silent link between hyperinsulinemia and gastric cancer.

This mechanistic review examined how hyperinsulinemia, common in obesity and preceding type 2 diabetes, contributes to gastric cancer risk and prognosis. It proposes that hyperinsulinemia promotes gastric oncogenesis by activating PI3K/AKT and MAPK/ERK signaling, including via insulin receptor isoform A overexpression and cooperating oncogenic alterations that drive proliferation, angiogenesis, and therapy resistance. The review highlights hyperinsulinemia as a metabolic driver of gastric cancer biology and suggests that targeting insulin signaling could be relevant for prevention and treatment strategies.

Laurenziello P, Luongo M, Lospinoso Severini F et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Hallmarks of epithelial-mesenchymal plasticity in cancer.

This article reviewed how epithelial-mesenchymal plasticity (EMP), including EMT, hybrid E/M states, and MET, enables cancer stem cell (CSC) transitions that drive metastasis and therapy resistance. It emphasizes that EMP is not a binary EMT/MET switch but a spectrum of intermediate phenotypes with increased tumorigenicity and metastatic potential. The scientific significance is that defining EMP “hallmarks” can identify actionable biomarkers and therapeutic strategies to disrupt CSC plasticity and resistance.

Clauzon L, Verona F, Shams K et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting ADAR1 lactylation activates innate immune and overcomes chemoresistance in ovarian cancer.

The study investigated whether ADAR1 lactylation-driven A-to-I RNA editing contributes to cisplatin chemoresistance in ovarian cancer. In cisplatin-resistant models, ADAR1 expression and global A-to-I editing were elevated, and ADAR1 knockdown increased cisplatin sensitivity while activating innate immune MAVS/PKR pathways and promoting CD4+ and CD8+ T-cell infiltration. Mechanistically, Tip60 mediated ADAR1 lactylation to enable interaction with the deubiquitinase USP48 for ADAR1 stabilization, linking a specific post-translational modification to immune activation and reversal of chemotherapy resistance.

Cui L, Yi Q, Tang C et al. · Cell death and differentiation · (2026) · View on PubMed ↗

GSDME acts as an epigenetic modifier to promote melanoma development via centriole biogenesis regulator PLK4.

This study examined a non-pyroptotic role for the gasdermin family member GSDME in melanoma development and its relationship to centriole biogenesis. The authors found that GSDME functions as an epigenetic modifier that promotes melanoma by regulating PLK4, a centriole biogenesis regulator, and that GSDME is upregulated in melanoma via promoter hypomethylation. These findings suggest that GSDME can drive tumor progression through epigenetic control of PLK4 rather than only through canonical pyroptosis, identifying a potential melanoma-specific regulatory axis.

Du J, Yang Y, Zhao M et al. · Cell death and differentiation · (2026) · View on PubMed ↗

Copper depletion boosts CNS leukemia therapy by inhibiting nucleotide synthesis through impairment of mitochondrial complex IV activity.

This study investigated how copper depletion can improve therapy for central nervous system (CNS) leukemia by targeting metabolic dependencies. Using a targeted in vivo CRISPR screen in systemic and CNS acute lymphoblastic leukemia (ALL) xenografts, the authors found that copper depletion—via genetic deletion of the copper transporter SLC31A1 or dietary intervention—slowed growth in both settings. Mechanistically, copper depletion impaired mitochondrial complex IV activity, reducing nucleotide synthesis and thereby suppressing leukemia proliferation, supporting a metabolism-targeted strategy for CNS-directed leukemia treatment.

Wong AYL, Myers JW, Prakash G et al. · Nature cancer · (2026) · View on PubMed ↗

Dehydration promotes intracellular lipid synthesis and accumulation.

This cellular study tested whether dehydration/hypertonic stress directly regulates lipid synthesis and metabolism, focusing on oxygen consumption and carbon source utilization. Hypertonic stress decreased cellular oxygen consumption, increased intracellular lipid synthesis, and promoted glutamine oxidation as a carbon precursor for lipid synthesis through remodeling mitochondrial metabolism. The work is significant because it provides a mechanistic link between water availability and lipid storage, explaining how dehydration can drive intracellular lipid accumulation.

Carty JS, Selvasingh J, Zuchowski Y et al. · Nature communications · (2026) · View on PubMed ↗

Huoxue Jiedu formula attenuates myocardial ischemia-reperfusion injury by modulating LAPTM4B/mTORC1/TFEB pathway-mediated autophagic flux.

Huoxue Jiedu Formula (HXJDF), a traditional Chinese medicine prescription, was tested in myocardial ischemia–reperfusion injury (MIRI) models to determine whether it restores autophagic flux. HXJDF attenuated MIRI by modulating the LAPTM4B/mTORC1/TFEB pathway, thereby improving autophagy-related processes implicated in injury. This mechanistic pathway-level evidence supports HXJDF as a candidate cardioprotective therapy targeting impaired autophagic flux.

Liao F, Yang W, Shi J et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Mitochondrial Carrier SLC25A13 Drives Ferroptosis Resistance and Immune Evasion via a STAT3-IFI6 Circuit in Breast Cancer.

This study investigated how the mitochondrial aspartate/glutamate carrier SLC25A13 regulates ferroptosis and antitumor immunity in triple-negative breast cancer (TNBC). SLC25A13 was upregulated in breast cancer, predicted poor prognosis with reduced CD8+ T-cell infiltration, and promoted tumor growth while suppressing ferroptosis and weakening CD8+ T-cell cytotoxicity through a STAT3–IFI6 circuit involving enhanced complex I-linked oxidative phosphorylation and reduced mitochondrial ROS. These findings suggest targeting SLC25A13/STAT3 signaling could both restore ferroptosis and improve immune responsiveness in TNBC.

Zhu Y, Tang Y, Chen Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Cell death pathways (ferroptosis, apoptosis, pyroptosis, etc.) & therapy resistance

An HDAC4-specific PROTAC degrader achieves radiation sensitization by enhancing ferroptosis in lung cancer.

This study investigated how HDAC4 regulates radiation response and ferroptosis in lung cancer, using CRISPR screening in patient-derived organoids and mechanistic assays of SUMOylation. The authors found that HDAC4 acts as an E3 SUMO ligase that SUMOylates MBD1, stabilizing MBD1 and repressing TP53 and CYP1A1 transcription to suppress lipid ROS formation and ferroptosis, and they developed an HDAC4-specific PROTAC (TP1) that sensitized tumors to radiation by enhancing ferroptosis. These findings identify the HDAC4–MBD1–TP53/CYP1A1 axis as a driver of radioresistance and support HDAC4-targeted PROTAC degradation as a potential radiosensitizing strategy in lung cancer.

Cheng C, Sun L, Yang J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Kaempferol functionally reprograms CD47 signaling to promote cytoprotection and attenuate oxeiptosis in severe acute pancreatitis.

The study investigated kaempferol (KA) as a cytoprotective agent in severe acute pancreatitis (SAP) using gain-/loss-of-function experiments in vitro and PAC-specific CD47 SAP mouse models. KA was found to functionally reprogram CD47 signaling to promote cytoprotection and attenuate oxeiptosis (a regulated cell death process) in pancreatic acinar cells. Mechanistically targeting the CD47 pathway with KA suggests a potential therapeutic strategy for limiting acinar cell loss in SAP.

Tian Y, Zhang Y, Gao Q et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Tirzepatide Versus Intensified Conventional Care After 2 Years of Treatment in Early Type 2 Diabetes : A Randomized Clinical Trial.

In the SURPASS-EARLY phase 4 randomized clinical trial, participants with early type 2 diabetes inadequately controlled on diet/exercise and metformin were assigned to tirzepatide versus intensified conventional care (ICC). After 2 years, tirzepatide produced superior glycemic outcomes with an acceptable safety profile compared with ICC. These results strengthen the case for early initiation of tirzepatide to achieve more durable control in early T2D.

Del Prato S, Heine RJ, Pérez Manghi FC et al. · Annals of internal medicine · (2026) · View on PubMed ↗

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Targeted drug delivery platforms (ADCs/AOCs/nanomaterials) & translational modeling

Recent advances in stimuli-responsive nanomaterials for the treatment of acute kidney injury.

This review synthesized current advances in stimuli-responsive nanomaterials for treating acute kidney injury (AKI) across major etiologies such as ischemia-reperfusion, sepsis, and drug-induced nephrotoxicity. It highlights convergent AKI pathophysiology—early microcirculatory dysfunction and renal tubular energy/mitochondrial failure—and maps how responsive nanoplatforms aim to deliver therapeutics to these actionable hubs. The review’s significance is to guide rational design of next-generation AKI nanomedicines that can respond to local injury cues and improve translational efficacy.

Chen S, Yu L, Wu L et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Research progress and development strategies of antibody-oligonucleotide conjugates.

This review article examined the development strategies and scientific rationale for antibody–oligonucleotide conjugates (AOCs), focusing on how nucleic-acid payloads enable gene regulation for extrahepatic delivery compared with antibody–drug conjugates (ADCs). It reports that AOCs have advanced for diseases such as Duchenne muscular dystrophy (DMD) to Phase III, but development is constrained by limited validated targets (e.g., TfR1) and strong dependence on antibody choice, linker design, and payload modification. These insights are significant for guiding next-generation AOC engineering to expand targetability and improve efficacy/safety for genetic disorders.

Fan W, Luan W, Yu W et al. · Gene therapy · (2026) · View on PubMed ↗

Pathophysiological and Molecular Features of DXd ADC-Related Interstitial Pneumonitis in Cynomolgus Monkeys.

This preclinical translational study investigated the pathophysiology of deruxtecan (DXd) antibody-drug conjugate (ADC)-related interstitial pneumonitis (ILD) using a reproducible cynomolgus monkey model. Weekly intravenous administration of a target-nonbinding human IgG1 DXd ADC for 12 weeks induced interstitial pneumonitis in all animals, with radiologic abnormalities emerging by week 6, and the study integrated bronchoalveolar lavage fluid (BALF) extracellular vesicle (EV) proteomics with lung single-cell RNA sequencing (scRNA-seq). These data aim to identify mechanistic biomarkers and cellular pathways that can improve prediction and mitigation of DXd ADC pulmonary toxicity.

Kumagai K, Iguchi T, Kubota K et al. · Cancer science · (2026) · View on PubMed ↗ · Free PDF ↗

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Biomarkers, risk stratification & clinical prediction

EASL-AASLD Delphi consensus statement on surrogate endpoints and real-world evidence in primary biliary cholangitis.

This EASL–AASLD Delphi consensus statement studied surrogate endpoints and the use of real-world evidence in primary biliary cholangitis (PBC) drug development. It identified key gaps—such as reliance on liver biochemistry and non-invasive fibrosis measures not accepted as validated efficacy endpoints, limited integration of real-world data, and lack of harmonized patient-reported outcome (PRO) use—and proposed consensus approaches to address them. The statement is clinically significant because it aims to improve endpoint validation and evidence generation for regulatory approval of PBC therapies.

Journal of hepatology · (2026) · View on PubMed ↗

Vascular Contributions to Cognitive Impairment and Brain Health: Clinical Update and Mechanistic Considerations: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement reviewed and synthesized evidence on vascular contributions to cognitive impairment and dementia, updating the 2011 statement and outlining mechanistic considerations and research gaps. The key finding was a consolidated view that vascular risk factors and vascular pathology interact with neurodegenerative processes in a causal pathway, supporting vascular risk reduction as a therapeutic target. Scientifically and clinically, it guides future studies and informs clinicians and researchers on how to integrate vascular mechanisms into prevention and treatment strategies for cognitive decline.

Sorond FA, Gorelick PB, Bae HJ et al. · Stroke · (2026) · View on PubMed ↗

Beyond aldosterone and renin: emerging biomarkers for diagnosing and subtyping primary aldosteronism.

This narrative review summarized emerging biomarkers and approaches for diagnosing and subtyping primary aldosteronism (PA) beyond traditional aldosterone and renin measurements. The key finding was that conventional aldosterone/renin ratio testing has limitations due to intra-individual variability and medication/diet/posture effects, motivating biomarker strategies that improve diagnostic accuracy and subtype classification. Clinically, better biomarkers could reduce missed PA diagnoses and improve selection of patients for targeted therapies such as adrenalectomy or mineralocorticoid receptor antagonists.

Libianto R, Uniacke CL, Fuller PJ et al. · Endocrine reviews · (2026) · View on PubMed ↗

Outcomes of Hormone receptor-positive/HER2-negative early breast cancer patients by risk of recurrence groups focusing on the intermediate-risk group: Retrospective analysis from GEICAM studies.

This retrospective analysis assessed outcomes in hormone receptor-positive/HER2-negative early breast cancer patients stratified by risk of recurrence, with emphasis on the intermediate-risk group, using data from GEICAM trials and the El Álamo IV registry. The study evaluated how real-world recurrence outcomes differed across risk groups and in the intermediate-risk subset in the context of contemporary endocrine therapy strategies (including regimens that incorporate CDK4/6 inhibitors such as abemaciclib or ribociclib). The results aim to inform long-term relapse-risk decision-making for adjuvant therapy selection beyond the short follow-up of pivotal trials.

Servitja S, Carrasco E, Andrés R et al. · Breast cancer research : BCR · (2026) · View on PubMed ↗ · Free PDF ↗

A visual analysis of the research dynamics of biomarkers for lung cancer screening.

This bibliometric study used Web of Science Core Collection records to map global research dynamics on biomarkers for lung cancer screening, integrating visual analytics and topic modeling (CiteSpace, VOSviewer, KH Coder, and LDA). The authors identified collaboration patterns, research hotspots, and emerging themes/burst periods to forecast future directions in lung cancer screening biomarker development. Scientifically, the work helps prioritize areas where new biomarker evidence is likely to accelerate, supporting more efficient planning of translational lung cancer screening research.

Zhu H, Li B, Kong R et al. · Clinical epigenetics · (2026) · View on PubMed ↗ · Free PDF ↗

Shared genetic architecture between depression and migraine: a large-scale genome-wide cross-trait analysis.

This large-scale genome-wide cross-trait analysis studied shared genetic architecture between depression (including postpartum depression, PPD) and migraine subtypes using summary statistics. Using linkage disequilibrium score regression (LDSC) and GNOVA, the authors estimated genetic correlations and identified pleiotropically associated loci across depression and migraine phenotypes. The significance is that it clarifies common biological pathways underlying comorbidity and may support future risk prediction and mechanistic studies for PPD–migraine overlap.

Zhang M, Li Q, Zhao Y et al. · The journal of headache and pain · (2026) · View on PubMed ↗ · Free PDF ↗

Exome-wide association study of blood lipids in 1,158,017 individuals from diverse populations.

This exome-wide association study analyzed rare coding variants affecting blood lipid traits in 1,158,017 individuals from diverse ancestries. Testing 2,997,401 rare coding variants, the authors identified 800 exome-wide significant associations (including 176 predicted loss-of-function and 624 missense variants) enriched for functional variant classes with additive and recessive effects relevant to genetic dyslipidemia and coronary artery disease (CAD) risk. The results provide a large-scale catalog of rare coding alleles that can improve molecular diagnosis and refine causal pathways for lipid-related CAD.

Koyama S, Yu Z, Choi SH et al. · Nature genetics · (2026) · View on PubMed ↗

Metabolic and inflammatory biomarker trajectories after a cancer diagnosis and the risk of cardiovascular diseases.

This cohort study (1985–2020) analyzed post-cancer biomarker trajectories in relation to subsequent cardiovascular disease (CVD) risk, using latent class growth modeling for 11 biomarkers and Cox regression for CVD outcomes. It found that patients with initially high and then increasing glucose levels had a 110% higher CVD risk than those with low-stable glucose, and that low-stable albumin—even within the normal range—was associated with elevated CVD risk (rest truncated). Clinically, trajectory-based biomarker stratification could improve CVD risk prediction and monitoring in cancer survivors beyond single time-point measurements.

Park H, Wang Q, Liu Q et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Regional heterogeneity in phenotypic and genetic associations between bone and brain in humans.

This human study assessed bone–brain associations across anatomical regions using structural imaging and genetic data from ~45,000 UK Biobank participants. The authors found widespread structural correlations between bone and brain phenotypes (34.9% of tested pairs significant) with pronounced regional heterogeneity in effect sizes that aligned with cortical development and evolutionary expansion gradients. Scientifically, it refines the bone–brain relationship by showing that associations are not uniform across the body/brain, which can guide more targeted genetic and mechanistic investigations of skeletal–neuropsychiatric comorbidity.

Zhao L, Tang Y, Zhao W et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Current application and future directions for the sarcopenic obesity Global Leadership Initiative (SOGLI) diagnostic algorithm.

This narrative review assessed how the Sarcopenic Obesity Global Leadership Initiative (SOGLI) diagnostic algorithm has been applied in adults (≥18 years) across studies published from 2022 to August 2025. It identified strengths and limitations of the algorithm’s screening, diagnostic assessment, and staging workflow and highlighted areas needing refinement. The review informs standardization of sarcopenic obesity diagnosis and improves comparability of future clinical research.

Minnetti M, Pierantozzi G, Aubertin-Leheudre M et al. · Clinical nutrition (Edinburgh, Scotland) · (2026) · View on PubMed ↗ · Free PDF ↗

Safety and efficacy of liposomal iron for iron deficiency anemia in pediatric population: A systematic review and meta-analysis of randomized controlled trials.

This systematic review and meta-analysis of randomized controlled trials assessed the efficacy and safety of liposomal iron versus conventional oral iron formulations for iron deficiency anemia (IDA) in children. The authors pooled pediatric RCT evidence to evaluate outcomes including hematologic response and gastrointestinal tolerability. The findings inform pediatric treatment selection by clarifying whether liposomal iron improves efficacy and reduces adverse effects compared with standard oral iron.

Alharran AM, Almutairi EY, Alazemi WB et al. · European journal of pediatrics · (2026) · View on PubMed ↗

Functional bowel disorders in idiopathic Parkinson’s disease: a Rome IV-based controlled study.

This Rome IV-based controlled cross-sectional study evaluated the prevalence and correlates of functional bowel disorders (FBDs) in 64 patients with idiopathic Parkinson’s disease (iPD) compared with 64 non-neurologic controls. FBD prevalence and associations with non-motor symptoms, mood, and quality of life were analyzed using the Rome IV Diagnostic Questionnaire plus NMSS, Hamilton scales, PDQ-39, and GIQLI (results truncated in the abstract). The findings are intended to clarify how functional gastrointestinal symptoms fit into the non-motor burden of iPD and to guide clinical assessment using standardized Rome IV criteria.

Yavuz Z, Uzun M, Mutlu T et al. · Neurodegenerative disease management · (2026) · View on PubMed ↗

Eye pain and ocular surface characteristics in Postural Orthostatic Tachycardia Syndrome (POTS): The role of autonomic dysfunction.

This retrospective observational study characterized eye pain and ocular surface findings in patients with postural orthostatic tachycardia syndrome (POTS) to determine whether symptoms reflect classic dry eye disease or autonomic dysfunction–related sensory changes. POTS patients who underwent standardized ocular surface evaluations at a tertiary center (2019–2024) were assessed with pain ratings and ocular surface measures (specific results truncated in the abstract). The clinical significance is that it may help distinguish neuropathic/autonomic ocular pain from tear-film–driven dry eye, guiding more targeted management of ocular symptoms in POTS.

Karakus S, Huang JJ, Yashar M et al. · The ocular surface · (2025) · 1 citations · View on PubMed ↗

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Cardiovascular disease prevention, lipids & atherosclerosis

In Vivo Base Editing of PCSK9 with VERVE-102 for Hypercholesterolemia.

This phase 1, open-label, single-ascending-dose study tested the investigational base-editing therapy VERVE-102 in adults with heterozygous familial hypercholesterolemia or premature coronary artery disease to durably inactivate hepatic PCSK9. The key finding was that a single intravenous infusion of VERVE-102 produced dose-dependent reductions in PCSK9 activity/LDL cholesterol consistent with effective in vivo base editing of PCSK9 in the liver. Scientifically and clinically, this supports base editing as a potentially durable, one-time therapeutic strategy for lowering LDL cholesterol by targeting PCSK9 at the DNA level.

Vafai SB, Täubel J, Ashdown T et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Obicetrapib and lipoprotein(a) levels in patients at high cardiovascular risk: a pooled analysis of trials.

This pooled analysis of randomized trials evaluated the lipoprotein(a) [Lp(a)]-lowering effect of the cholesteryl ester transfer protein (CETP) inhibitor obicetrapib 10 mg daily versus placebo over 12 weeks in high cardiovascular risk patients with heterozygous familial hypercholesterolemia (HeFH) or atherosclerotic cardiovascular disease (ASCVD). In 2356 participants, obicetrapib produced clinically meaningful reductions in Lp(a) compared with placebo. These data strengthen the evidence base for CETP inhibition as an Lp(a)-targeting strategy in patients at elevated cardiovascular risk.

Nicholls SJ, Nelson AJ, Ray KK et al. · European heart journal · (2026) · View on PubMed ↗ · Free PDF ↗

Lipoprotein(a) Levels, Risk of Cardiovascular Events and Benefit of Evolocumab: Findings From the VESALIUS-CV Trial.

This prespecified analysis of the VESALIUS-CV trial studied whether baseline lipoprotein(a) [Lp(a)] levels identify higher cardiovascular risk and predict greater benefit from evolocumab in patients with qualifying atherosclerosis or high-risk diabetes but without prior myocardial infarction or stroke. In 7557 randomized participants followed for a median of 4.6 years, Cox models assessed adjusted cardiovascular event risk across baseline Lp(a) strata in the placebo arm and the interaction with evolocumab benefit (details truncated in the abstract). Clinically, the work aims to refine patient selection for PCSK9 inhibition by using Lp(a) as a risk and treatment-response biomarker in primary-prevention–like populations.

Monguillon V, Marston NA, Bohula EA et al. · Circulation · (2026) · View on PubMed ↗

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Cardiovascular complications after MI & vascular remodeling

Pulsed Field Ablation Versus Sham to Treat Atrial Fibrillation: The PFA-SHAM Randomized Clinical Trial.

This randomized clinical trial compared pulsed field ablation (PFA) versus sham procedures in symptomatic atrial fibrillation patients using a prospective, sham-controlled, single-blind design with blinded endpoint assessment. The key finding was that PFA’s clinical outcomes for atrial fibrillation recurrence and subjective endpoints were evaluated against placebo effects using the sham control to address prior unblinded trial limitations. The significance lies in providing higher-quality evidence on the true efficacy and patient-centered impact of PFA by separating treatment effects from placebo and expectation effects.

Osmancik P, Neuzil P, Hozmanova J et al. · Circulation · (2026) · View on PubMed ↗

Pathophysiology, prevention, and management of coronary microvascular obstruction.

This European Heart Journal review synthesized current knowledge on the pathophysiology, prevention, and management of coronary microvascular obstruction after STEMI. It emphasizes that even with prompt primary PCI, microvascular obstruction and ischemia–reperfusion injury drive the no-reflow phenomenon in up to ~60% of cases, worsening infarct healing, left ventricular remodeling, and risk of heart failure and death. The review is clinically significant because it frames microvascular obstruction as a key therapeutic target to improve post-infarction outcomes despite successful epicardial reperfusion.

Cenko E, Badimon L, Vadalà G et al. · European heart journal · (2026) · View on PubMed ↗

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Diabetes, obesity & cardiometabolic disease mechanisms

Ketogenic Diet Might Regulate Autophagy of BMSCs via mTOR Signaling Contributing to Osteoporosis in Mice.

This mouse study tested whether a ketogenic diet (KD) contributes to osteoporosis by regulating autophagy in bone marrow stromal cells (BMSCs) through mTOR signaling, and evaluated the effects of the mTOR inhibitor rapamycin (Rapa). The key finding was that KD-induced bone loss was associated with altered autophagy markers (including LC3) and that modulating mTOR with rapamycin could counteract aspects of KD-driven osteoporosis-related changes. This is significant because it links dietary ketosis to mTOR–autophagy biology in BMSCs, offering mechanistic targets for preventing or treating osteoporosis.

Liu Q, Yang Z, Ye Y et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of semaglutide on mortality, cardiovascular, and kidney outcomes across the cardio-kidney-metabolic continuum: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated randomized controlled trials comparing the GLP-1 receptor agonist semaglutide versus placebo to determine effects on all-cause and cardiovascular mortality and on major cardiovascular and kidney outcomes across the cardio–kidney–metabolic continuum. Across eligible RCTs, semaglutide showed prognostic benefits on mortality and cardiometabolic endpoints (with pooled estimates synthesized across diverse patient populations), extending prior trial findings beyond single-condition outcomes. Clinically, the analysis supports semaglutide as a therapy with broad outcome relevance for patients at risk spanning cardiovascular and kidney disease domains.

Marzano F, Paolillo S, Gargiulo P et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Shared pathophysiological mechanisms between diabetes and calcific aortic valve disease: an immunometabolic perspective.

This review examined shared immunometabolic mechanisms linking diabetes mellitus to accelerated calcific aortic valve disease (CAVD) and considered therapeutic implications. It synthesizes epidemiologic, imaging, and histologic evidence showing diabetes increases incident aortic stenosis risk and calcification severity and outlines seven interconnected pathways by which dysglycemia remodels CAVD pathobiology. The significance is to identify diabetes-driven targets that could enable disease-modifying strategies for CAVD in patients with diabetes.

Yue Z, SiTu Q, Bian JH et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

A prospective study of physical activity and cardiometabolic diseases in association with cancer risk.

This study meta-analyzed individual participant data from 598,890 adults (35–70 years) across EPIC and UK Biobank to assess how non-occupational physical activity relates to cancer risk in people with and without cardiometabolic disease (cardiovascular disease and/or type 2 diabetes). The abstract is truncated before reporting the key quantitative findings, but the analysis framework uses prospective cancer incidence with stratification by cardiometabolic status. Scientifically, it aims to clarify whether physical activity’s cancer-preventive effects differ by cardiometabolic comorbidity, which could inform risk-tailored prevention strategies.

Gebremariam A, Fontvieille E, Gan Q et al. · Communications medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Serum uric acid, gout, cardiometabolic diseases, and multimorbidity: a prospective cohort study using multi-state model.

This prospective cohort study examined associations between serum uric acid (SUA), gout, and cardiometabolic multimorbidity trajectories in over 400,000 UK Biobank participants using a multi-state model. SUA and gout were analyzed for their roles in transitions from cardiometabolic disease–free status to first cardiometabolic disease and subsequent multimorbidity progression. The results are clinically significant because they clarify whether SUA and gout are not only risk markers but also trajectory-shaping factors for cardiometabolic multimorbidity, informing prevention and risk stratification.

Wu C, Zhong G, Yang Y et al. · npj aging · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 receptor agonists at the crossroads of obesity and addiction: A review of shared neurobiology and translational evidence.

This narrative review examined how glucagon-like peptide-1 receptor agonists (GLP-1 RAs) intersect obesity and addiction by comparing shared neurobiology and translational evidence. It argues that GLP-1 RAs act on both peripheral metabolic pathways and central reward circuitry, positioning them as potential adjunctive treatments for substance use disorders. The scientific significance lies in proposing a mechanistic bridge between obesity and addiction that could accelerate repurposing and guide future translational trials.

Lista S, Ballerio M, López-Ortiz S et al. · Pharmacology, biochemistry, and behavior · (2026) · View on PubMed ↗

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Inflammation, immune regulation & host-microbe interactions

Gut Microbiota Regulates Systemic Inflammatory Response and Compensatory Anti-Inflammatory Response Syndromes by Targeting PF4+ Macrophages in Acute Pancreatitis.

This study investigated how gut microbiota modulates systemic inflammatory response syndrome (SIRS) and compensatory anti-inflammatory response syndrome (CARS) in acute pancreatitis (AP) by targeting PF4+ macrophages. It found that AP patients and mouse models show reduced Bacteroides thetaiotaomicron abundance, which increases PF4+ macrophage infiltration and promotes Th2-cell recruitment, thereby shaping the SIRS/CARS immune balance. The results are significant because they connect a specific microbiome change to macrophage-driven immune remodeling, highlighting PF4+ macrophages as a mechanistic therapeutic target in AP.

Liu L, Li G, Lu D et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Large-scale meta-analysis of infection risk with JAK-STAT inhibitors in 29,000 patients.

This study performed a systematic review and large-scale meta-analysis of randomized controlled trials evaluating infection risk associated with Janus kinase (JAK)-STAT inhibitors in approximately 29,000 patients with immune-mediated inflammatory diseases of the skin (e.g., atopic dermatitis, alopecia areata, vitiligo). The key finding was that JAK-STAT inhibitors showed an overall infection risk signal that could be comprehensively characterized across reported infection types, including comparisons between systemic and topical agents rather than only pre-specified categories. Clinically, these results help refine infection-risk counseling and risk–benefit decisions for dermatologic use of JAK-STAT inhibitors by providing a more complete, head-to-head style synthesis of trial infection outcomes.

Krebs M, Gulyás L, Fazekas KK et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗

Exercise hormone irisin alleviates rheumatoid arthritis by removing dysfunctional mitochondria.

The study investigated whether the exercise hormone irisin can treat rheumatoid arthritis in mouse models (K/BxN serum-induced arthritis and collagen-induced arthritis) and explored the mechanism involving ITGAV/ITGB5-driven mitophagy and clearance of leaked mitochondrial DNA. Irisin interacted with integrin subunits ITGAV and ITGB5 to activate mitophagy, reduce leaked mtDNA and reactive signals, and thereby alleviate inflammatory arthritis phenotypes. These results suggest a mechanistic bridge between exercise and RA therapy via integrin-mediated mitochondrial quality control, supporting irisin/mitophagy pathways as potential therapeutic targets.

Wu Y, Fu T, Teng Y et al. · Autophagy · (2026) · View on PubMed ↗

Systemic implications of osteoarthritis: from local degeneration to systemic metabolic Dysregulation.

This review synthesized evidence that osteoarthritis (OA) is not only a local joint degeneration process but also involves systemic metabolic and inflammatory dysregulation. It links local mechanisms such as synovial macrophage polarization, mitochondrial dysfunction, and autophagy defects to a pro-inflammatory milieu and “spillover” of cytokines (e.g., IL-1β, TNF-α) and extracellular vesicles that may affect whole-body physiology. The reframing supports systemic biomarkers and multi-organ therapeutic approaches for OA rather than purely local interventions.

Luo J, Li L, Deng Q et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

GPR161 contributes to macrophage glycolytic reprogramming via targeting C5aR1 in acute lung injury.

This study investigated how GPR161 regulates macrophage glycolytic reprogramming through targeting C5aR1 in acute lung injury (ALI) and ARDS. It found elevated GPR161 expression in peripheral circulating monocytes from ARDS patients that correlated with disease severity, and it used genetically engineered mouse models to test the GPR161–C5aR1 axis in macrophage metabolic and inflammatory responses. The significance is identifying a tractable signaling pathway (GPR161→C5aR1→glycolysis) that could be targeted to modulate macrophage-driven inflammation in ARDS.

Li YH, Yang X, Chen Y et al. · Cellular & molecular biology letters · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondrial flagella-like extensions (MitoFLARE) dysfunction triggers STING-mediated immune dysregulation in sepsis.

This mechanistic study examined how mitochondrial flagella-like extensions (MitoFLARE) dysfunction triggers STING-mediated immune dysregulation in sepsis, using early-stage LPS treatment models. It showed that mitochondria remodel by extruding mitoFLARE during early LPS exposure, with formation driven by glycosylated TRAK1 binding FHL2 to promote actin network formation, linking mitochondrial DNA (mtDNA) release to immune dysregulation (text truncated). The significance is that it identifies a mitochondrial communication pathway upstream of STING activation, offering potential targets to modulate harmful immune responses in sepsis.

Hong W, Ma R, Long S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanistic basis of teichoic acid transport by a gatekeeper flippase.

This structural and mechanistic study investigated how the gatekeeper flippase TacF transports phosphocholine-containing teichoic acids in Streptococcus pneumoniae. Using a cryo-EM structure of TacF in lipid nanodiscs plus in vivo complementation assays and molecular dynamics simulations, it identified key residues involved in teichoic acid recognition and transport (text truncated). The work is significant because it reveals the molecular basis of a bacterial cell-wall transport step that supports colonization and immune evasion, informing potential antibacterial target development.

Cebrero G, Chidananda AH, Cester E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

GPSM1 restricts CD73+CD103+ Treg cells in adipose tissue, critical for promoting obesity-related metabolic deterioration.

This study investigated the role of G-protein-signaling modulator 1 (GPSM1) in CD4+ T cells and adipose tissue regulatory T (Treg) cell subsets in humans and mice, including genomic deletion experiments and metabolic phenotyping under high-fat diet. GPSM1 expression increased in obesity and glucose dysregulation, and deleting GPSM1 in CD4+ T cells or Treg cells expanded CD73+CD103+ Treg cells, reduced adipose inflammation, and improved insulin and glucose tolerance in high-fat-fed mice. These findings suggest GPSM1 as a mechanistic regulator of a specific pro-metabolic Treg subset and a potential therapeutic target to mitigate obesity-related metabolic deterioration.

Lyu XR, Qi RB, Hua YL et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Human infection with Andes hantavirus: an update for the general physician.

This narrative update reviewed Andes hantavirus (ANDV) infection in humans, focusing on transmission, incubation, clinical spectrum, and particularly hantavirus cardiopulmonary syndrome (HCPS). It highlights ANDV’s distinctive ability for sustained human-to-human transmission via respiratory droplets and close contact, with incubation reported as 9–40 days and a median reproductive number >2, and it summarizes the feared HCPS manifestations including acute respiratory failure and multi-organ involvement. The review is significant for general clinicians because it consolidates practical knowledge on recognition and risk of ANDV infection, which is essential for timely diagnosis and management.

Durante-Mangoni E, Cafarella I, Mercadante S et al. · European journal of internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Pairwise Comparative Safety and Effectiveness of Anti-TNF Blockers, Vedolizumab, and Ustekinumab During Pregnancy: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis compared pairwise safety and effectiveness of anti-TNF blockers versus vedolizumab (VDZ) and ustekinumab (UST) during pregnancy in patients with inflammatory bowel disease (IBD). Across included studies through July 2025, pooled analyses estimated relative risks for maternal and neonatal outcomes using random-effects risk ratios. The results help clinicians counsel pregnant IBD patients by clarifying comparative risks and benefits among biologic classes.

Segun-Omosehin O, Bourdakos NE, Tzanis KG et al. · Digestive diseases and sciences · (2026) · View on PubMed ↗

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Pulmonary disease (ALI/ARDS, ILD, COPD/asthma/bronchiectasis, pulmonary hypertension)

Hypoxia Upregulation of BACH1 Aggravates Pulmonary Hypertension Through TGFBR2/SMAD Pathways.

This study investigated how hypoxia-induced upregulation of the transcription factor BACH1 contributes to pulmonary hypertension via TGFBR2/SMAD signaling using coimmunoprecipitation, cultured pulmonary artery smooth muscle cells, rodent pulmonary hypertension models, patient specimens from idiopathic pulmonary arterial hypertension, and single-nucleus RNA sequencing. The key finding was that BACH1 was upregulated under hypoxic conditions and aggravated pulmonary hypertension through activation of the TGFBR2/SMAD pathway. Clinically, identifying the BACH1–TGFBR2/SMAD axis highlights a mechanistic target for developing therapies to limit vascular remodeling in pulmonary hypertension.

Hou Y, Li Q, Wei TW et al. · Circulation · (2026) · View on PubMed ↗

Relationship between negative-pressure ICU rooms and the risk of COVID-19-associated pulmonary aspergillosis: an ancillary analysis of the COVID-ICU cohort study.

This ancillary analysis of the prospective multicenter COVID-ICU cohort studied whether environmental negative-pressure ICU rooms affect the risk of COVID-19-associated pulmonary aspergillosis (CAPA) among 1,233 mechanically ventilated patients. The analysis compared CAPA incidence between patients exposed to different ICU room air-pressure conditions and assessed the association between negative-pressure rooms and CAPA risk. If confirmed, the findings would have practical infection-control implications by identifying an environmental risk modifier for CAPA in critically ill SARS-CoV-2 patients.

Kreitmann L, Rouzé A, Luyt CE et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Structured Exercise Regimen in Pulmonary Hypertension-Right Ventricular Failure in an Ovine Model.

An ovine model of chronic pulmonary hypertension–right ventricular failure (PH-RVF) was used to test the effects of a structured exercise regimen on disease physiology under exercise-induced stress. Eight Dorset cross sheep underwent PH-RVF induction via left pulmonary artery ligation and progressive main pulmonary artery occlusion, with pressure monitoring via tunneled lines and an eight-week exercise protocol. This provides a controlled large-animal platform to study how exercise modulates PH-RVF progression and right-heart failure mechanisms.

Bulard BA, Kumpfbeck AR, Woo Y et al. · Journal of visualized experiments : JoVE · (2026) · View on PubMed ↗

Chest CT imaging toward personalized management of chronic obstructive pulmonary disease, asthma, and bronchiectasis: pulmonologist perspectives.

This narrative review synthesized pulmonologist perspectives on using chest computed tomography (CT) for personalized management of chronic obstructive pulmonary disease (COPD), asthma, and bronchiectasis. It emphasizes that CT enables quantitative and qualitative assessment of emphysema, airway structure, mucus plugging, vascular abnormalities, bronchiectasis, and comorbid interstitial lung abnormalities, and discusses advances in CT image analysis relevant to phenotyping. The review supports CT-driven precision approaches to tailor management across chronic airway diseases.

Tanabe N, Hirai T · Japanese journal of radiology · (2026) · View on PubMed ↗

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Neurology: Parkinson’s disease & synucleinopathies

Irisin-integrin αV/β5 coupling of α-synuclein phagocytosis and clearance.

This study examined whether the exercise-inducible myokine irisin modulates α-synuclein (α-syn) clearance in Parkinson’s disease with cognitive impairment (PD-CI) and tested the receptor mechanism in human PD patients and microglia. Irisin increased circulating irisin levels, reduced serum α-syn, and improved cognition in 21 PD patients, while mechanistically signaling via integrin αV/β5 to enhance microglial α-syn phagocytosis and clearance, lowering α-syn burden. These findings support an irisin–integrin αV/β5 axis as a potential disease-modifying therapeutic target to reduce α-syn pathology in PD-CI.

Liu Y, Shi S, Zhang J et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Phenylalanyl-tRNA synthetase FARS-1/FARSA balances longevity and immunity by downregulating endogenous mitochondrial double-stranded RNAs.

This study investigated how phenylalanyl-tRNA synthetase FARS-1/FARSA regulates the balance between longevity and immunity by controlling endogenous mitochondrial double-stranded RNAs (dsRNAs) in Caenorhabditis elegans and cultured human cells. The authors found that dsRNA levels rise with aging and senescence, and that FARS-1/FARSA extends lifespan by downregulating mitochondrial dsRNAs through a previously unrecognized dsRNA-binding domain. These results are significant because they identify a mechanistic “moonlighting” role for FARS-1/FARSA in suppressing immunogenic mitochondrial dsRNA accumulation, linking RNA homeostasis to healthy aging.

Sohn J, Jeon M, Lee H et al. · Molecular cell · (2026) · View on PubMed ↗

CHCHD2 and CHCHD10 promoted autophagic clearance of protein aggregates via GABARAPs.

This mechanistic study examined how mitochondrial proteins CHCHD2 and CHCHD10 contribute to autophagic clearance of protein aggregates relevant to neurodegenerative disease. CHCHD2 and CHCHD10 formed a complex with C1QBP/p32 and ATG8-family proteins, preferentially engaging GABARAPs, and disease-associated CHCHD2/CHCHD10 mutations impaired this autophagy-related pathway (details truncated in the abstract). Scientifically, the work links CHCHD2/CHCHD10 to GABARAP-mediated autophagy, suggesting a potential molecular target to counter aggregate accumulation in Parkinson disease, ALS, FTD, and Alzheimer disease.

Wei Z, Zhang M, Tang W et al. · Autophagy · (2026) · View on PubMed ↗

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Neurology: Alzheimer’s disease & tau/mitochondrial transfer

Microglial mitochondria transfer to astrocytes via GPNMB-enriched extracellular vesicles alleviates cognitive deficits in tauopathy mice.

This study examined how microglia-derived glycoprotein nonmetastatic melanoma protein B (GPNMB) and mitochondria are transferred to astrocytes via extracellular vesicles (EVs) in PS19 tauopathy mice. It found that tau cleavage in microglia generates N-terminal fragments that form a Parkin/Nix–GPNMB complex on mitochondria, driving secretion of EVs carrying functional mitochondria that improve astrocytic function and attenuate cognitive deficits. These findings suggest a GPNMB/mitochondrial EV axis as a mechanistic and potentially targetable pathway to mitigate cognitive impairment in tau-driven neurodegeneration.

Liang C, Zhou Y, Zhuang K et al. · Nature neuroscience · (2026) · View on PubMed ↗

Loss of Brain-Derived Estrogen Is Associated With Sex- and Age-Dependent Alterations in Memory, Affective Behavior, and Hippocampal Extracellular Matrix Gene Expression.

This study used brain-specific aromatase knockout (bArKO) and whole-body total aromatase knockout (tArKO) mice of both sexes to model estrogen deficiency and assess effects on memory, affective behavior, and hippocampal extracellular matrix gene expression. The key finding was that loss of brain-derived estrogen produced sex- and age-dependent alterations in behavioral phenotypes and hippocampal extracellular matrix gene expression. These results are significant because they provide a mechanistic framework for how estrogen deficiency may contribute to sex differences in Alzheimer’s disease vulnerability.

Piehl NC, Halle AW, Rodriguez G et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Is SORL1 a common genetic target across neurodegenerative diseases? A multi-ancestry biobank study.

This multi-ancestry biobank study assessed whether genetic variation in SORL1 (encoding the SORLA protein) contributes to risk across neurodegenerative diseases using data from six large-scale biobanks totaling 15,043 Alzheimer’s disease cases, 9,943 related dementia cases, and additional Parkinson’s disease cohorts. The key finding was that SORL1 genetic associations were evaluated across Alzheimer’s disease, related dementias, and Parkinson’s disease to determine whether SORL1 is a shared genetic target beyond Alzheimer’s disease. Scientifically, clarifying cross-disease SORL1 involvement strengthens or refines the rationale for therapies aimed at restoring SORLA/retromer trafficking pathways.

Khani M, Yeboah SN, Cerquera-Cleves C et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Ketogenic diet as a therapeutic strategy for neurodegenerative diseases: from mechanisms to translational challenges.

This translational review summarized mechanistic evidence for the ketogenic diet (KD) as a therapeutic strategy in neurodegenerative diseases, focusing on how ketone bodies and metabolic shifts influence oxidative stress, inflammation, autophagy/protein aggregation, and the gut microbiome. The authors conclude that KD can modulate multiple disease-relevant pathways across disorders including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, while also addressing translational challenges for clinical implementation. Scientifically, the review frames KD as a multi-target metabolic intervention and highlights key gaps needed to move from mechanistic promise to reliable patient outcomes.

Salgueiro AM, Ferreira-Marques M, Ribeiro RFN et al. · Translational neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

Dysfunction of the CD38-Miro1 Axis Disrupts Astrocyte-neuron Mitochondrial Transfer in Alzheimer’s Disease: Mechanisms and Therapeutic Restoration.

This review summarizes mechanistic evidence in Alzheimer’s disease (AD) for how dysfunction of the astrocyte-to-neuron mitochondrial transfer pathway is driven by the CD38–Miro1 axis. It highlights that neuronal distress activates astrocytic CD38, producing cyclic ADP-ribose that triggers calcium release and disrupts Miro1-dependent mitochondrial trafficking, thereby impairing mitochondrial shuttling and bioenergetic compensation. The proposed pathway offers a therapeutic target for restoring mitochondrial transfer and improving neuronal resilience in AD.

Abdelaziz AM, Shokr MM, Fathy MK et al. · Journal of molecular neuroscience : MN · (2026) · View on PubMed ↗

Neocortical tau burden determines the degree of cognitive impairment in individuals with Braak stage V neurofibrillary degeneration.

This neuropathology study in individuals with Alzheimer disease neuropathologic change (ADNC) examined whether quantitative neocortical hyperphosphorylated tau (p-tau) burden predicts cognitive impairment severity among those with Braak stage V neurofibrillary degeneration. Using computer-assisted positive pixel quantification of neocortical p-tau, the authors found that neocortical tau burden better determined the degree of cognitive impairment than existing neuropathologic metrics alone. This improves the scientific basis for linking regional tau pathology to cognition and may refine prognostic assessment in AD.

Richardson TE, Cherry J, Kandoi S et al. · Acta neuropathologica · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurology: other neurodegeneration & CNS disorders (MSA, tauopathy circuits, epilepsy, etc.)

TPPP/p25 amyloid seeding activity as a specific biomarker for multiple system atrophy.

This study investigated tubulin polymerization promoting protein (TPPP/p25) as a cerebrospinal fluid (CSF) biomarker to specifically diagnose multiple system atrophy (MSA) by detecting disease-related α-synucleinopathy seeds. It found that native TPPP/p25 is self-protected against amyloid aggregation, whereas disease-related mutations disrupt this protection to trigger TPPP/p25 aggregation, with cryo-electron microscopy (cryo-EM) revealing structural changes in the core domain. The results are clinically significant because they propose a more disorder-specific CSF biomarker for differentiating MSA from other synucleinopathies than generic α-syn seed assays.

Zeng S, Zhang S, Zhang S et al. · Cell · (2026) · View on PubMed ↗

Effect of Electroacupuncture on Postherpetic Neuralgia: A Randomized Clinical Trial.

This multicenter randomized clinical trial studied whether electroacupuncture reduces pain severity in patients with postherpetic neuralgia (PHN) compared with sham electroacupuncture. It found that electroacupuncture was effective in lowering PHN pain severity while evaluating safety across 7 tertiary hospitals in China (participants enrolled 2020–2022). The trial is significant because it provides higher-quality evidence for electroacupuncture as a potential therapeutic option for a refractory neuropathic pain condition.

Chen L, Liu Q, Pei L et al. · JAMA neurology · (2026) · View on PubMed ↗

NINJ1 hypomethylation enhances endothelial dysfunction in brain arteriovenous malformations.

This study examined epigenetic dysregulation in brain arteriovenous malformations (bAVMs), focusing on NINJ1 DNA methylation and endothelial dysfunction in human bAVM nidus tissues. Using genome-wide DNA methylation profiling with the Illumina Infinium MethylationEPIC v2 (935K) array plus targeted pyrosequencing and immunofluorescence, it found that NINJ1 hypomethylation enhances endothelial dysfunction, supporting a mechanistic role for epigenetic changes in vascular fragility. The findings are significant for identifying NINJ1 methylation as a potential biomarker and therapeutic entry point in pediatric/young-adult bAVM pathogenesis.

Chen CJ, Zhang H, Pan T et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗

GABA signaling in NG2 glia mediates empathy-like behavior under observational social defeat.

This mouse study investigated how GABA signaling in NG2 glia mediates empathy-like behavior during observational social defeat (OSD), using whole-brain cFos mapping and fiber photometry to identify medial amygdala (MeA) circuits. OSD increased consolation-like allogrooming, and MeA GABAergic neuron activation correlated with empathic allogrooming; specific NG2 glia ablation in the MeA reduced inhibitory synaptic transmission and disinhibited behavior. The findings are significant because they mechanistically link NG2 glia–GABA signaling to social-cognitive behavior, suggesting glial modulation as a potential target for disorders involving impaired empathy.

Jian Y, Jin S, Liu P et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Epileptic and developmental encephalopathy secondary to inversion-duplication of chromosome 15: Description of epilepsy characteristics and therapeutic outcomes.

This retrospective multicenter study in 54 patients with chromosome 15 inversion-duplication syndrome (invdup15; 15q11.2–q13.1) across 37 Spanish hospitals characterized epilepsy phenotypes and treatment outcomes, comparing invdup15q versus intdup15q genetic subgroups. Patients showed highly prevalent, often drug-resistant epilepsy with progression toward developmental epileptic encephalopathy features such as Lennox-Gastaut syndrome, and the study linked epilepsy characteristics and EEG findings to therapeutic response. These data improve clinical phenotyping and may help guide more personalized antiseizure treatment strategies for invdup15-associated DEEs.

Benítez-Provedo C, García-Fernández M, Gutiérrez-Delicado E et al. · Epilepsia · (2026) · View on PubMed ↗

Brain Serotonin Deficiency Impairs Ovarian Reserve Function via the Hypothalamic-Pituitary-Ovarian Axis.

This study used brain-specific Tph2 conditional knockout (Tph2-CKO) mice to test whether brain-derived serotonin (5-HT) regulates ovarian reserve via the hypothalamic–pituitary–ovarian (HPO) axis. Loss of brain 5-HT reduced follicle numbers and anti-Müllerian hormone (AMH) levels, indicating diminished ovarian reserve, and mechanistic data implicated suppression of ovarian mTOR signaling. These findings support a causal role for central serotonin in female reproductive aging/infertility biology and suggest potential targets for preserving ovarian reserve.

Cui SS, Yang ZN, Xiao J et al. · Neuroscience bulletin · (2026) · View on PubMed ↗

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Epigenetics, RNA biology & chromatin regulation

Physics-based nucleosome-resolution modeling of epigenetic-driven chromatin domain dynamics.

This work developed a physics-based, nucleosome-resolution coarse-grained computational model to study how epigenetic marks and chromatin components drive chromatin domain dynamics across scales. The key finding was that the model can capture experimentally relevant effects of DNA linker length, histone tail acetylation, linker histone H1, and multibromodomain proteins such as BRD4, while also incorporating liquid–liquid phase separation and nucleosome-to-fiber folding. This is significant because it provides an experimentally accurate yet computationally efficient framework for simulating ~100 kb genomic regions to connect epigenetic regulation with 3D genome behavior.

Gu C, Takada S, Brandani GB · Nucleic acids research · (2026) · View on PubMed ↗ · Free PDF ↗

Kbhb Proteome Resource Reveals a Metabolic-Epigenetic Crosstalk Governing Rice Blast Resistance via OsACLA2 Activity Regulation.

This proteomics study profiled lysine β-hydroxybutyrylation (Kbhb) in rice leaves and tested how Kbhb regulates rice blast resistance through ATP-citrate lyase OsACLA2 activity, including the role of the “eraser” histone deacetylase OsHDA705. The authors identified 656 Kbhb sites on 482 proteins and found that Kbhb at conserved K262 of OsACLA2 enhances its enzymatic activity, which is required for full resistance because K262 mutants show compromised immunity. The work links metabolite-derived Kbhb to metabolic–epigenetic control of plant defense and highlights OsACLA2 K262 as a mechanistic target for improving resistance to Magnaporthe oryzae.

Fang Y, Li W, Zhou Y et al. · Journal of agricultural and food chemistry · (2026) · View on PubMed ↗

SUMOylation in cancer: molecular mechanisms and therapeutic implications.

This review summarized how SUMOylation (small ubiquitin-like modifier modification) regulates cancer cell-intrinsic behavior and the tumor immune microenvironment (TIME), with emphasis on immune evasion mechanisms. It reports that SUMOylation promotes immune escape by suppressing antigen presentation, narrowing immunopeptidome diversity, and modulating immune checkpoints including direct evidence for PD-L1 and TIGIT, and it discusses therapeutic inhibition approaches such as TAK-981. The clinical significance is that targeting SUMOylation could enhance anti-tumor immunity and improve responses to immunotherapies.

Ding Y, Li F, Wang JM · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

An encyclopedic regulatory and functional atlas of RNA interactomes.

The study developed an encyclopedic atlas of RNA interactomes by mapping RNA-RNA and RNA-binding protein (RBP)-RNA interactions. Using the rbsSeeker and rriScan tools integrated into ENCORI, the authors identified and validated novel N6-methyladenosine (m6A)-associated proteins, an orphan small nucleolar RNA that guides rRNA pseudouridines, and target-directed microRNA degradation events. This resource advances systematic discovery of RNA interactome biology and provides a framework for studying how RNA modifications and small RNAs rewire gene regulation.

Zhou K, Huang J, Liu S et al. · Nature methods · (2026) · View on PubMed ↗

HBV HBx protein masks epigenetic reader Spindlin1 via an inter-molecular zinc finger to subvert transcriptional control.

This study examined how Hepatitis B virus (HBV) HBx protein subverts host transcriptional control by masking the epigenetic reader Spindlin1, focusing on the HBx1-120 isoform and its interaction mechanism. Using an NMR-based residue-level interaction approach, the authors showed HBx1-120 is disordered alone but locally folds upon binding Bcl-xL and Spindlin1, forming a bivalent complex that uses an inter-molecular zinc finger to recruit and occlude Spindlin1. These structural and mechanistic insights are significant because they explain how HBx hijacks an epigenetic reader at the molecular level, informing antiviral strategies targeting HBx–host protein interactions.

Clavier A, Shida T, Droemer MA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Model systems, methods & translational research tools

EASL position paper on preclinical models of steatotic liver disease.

This EASL position paper studied how to define and use preclinical models for steatotic liver disease (SLD), including metabolic dysfunction-associated steatotic liver disease (MASLD), MetALD, alcohol-associated/related liver disease (ALD), and other causes such as drug-induced and monogenic etiologies. It concluded that current preclinical model selection and reporting should better reflect SLD heterogeneity and align with translational needs for evaluating steatohepatitis and fibrosis progression. The consensus is significant for improving the scientific rigor and regulatory relevance of preclinical SLD research.

Gallage S, Castro RE, Estall J et al. · Journal of hepatology · (2026) · View on PubMed ↗

Psilocybin induces stereotyped movements and reduces defensive responding in planarians through 5-hydroxytryptamine mechanisms.

The study examined whether psilocybin, a 5-HT2AR agonist, alters behavior in the planarian Dugesia dorotocephala and whether effects depend on 5-hydroxytryptamine signaling using the selective 5-HT2AR antagonist volinanserin. Psilocybin increased stereotyped movements (e.g., head bops, twists, scrunches, C-shapes) and reduced defensive responding (negative phototaxis), with the behavioral changes mediated by 5-HT2AR mechanisms. These findings support conserved serotonergic pharmacology for psilocybin across species and identify planarians as a tractable model to dissect 5-HT2AR-dependent behavioral effects relevant to anxiety-like and psychedelic-like phenotypes.

Akbar RJ, Stringer AD, Wiah S et al. · Behavioural pharmacology · (2026) · View on PubMed ↗

Construct optimization for AAV-mediated human α-syn overexpression, and validation across research settings: Development of a shared tool for the research community.

This study focused on optimizing and standardizing an AAV-mediated human α-synuclein (α-syn) overexpression model of Parkinson’s disease to reduce variability across research settings. The authors developed a shared construct optimization tool in collaboration with the Michael J. Fox Foundation for Parkinson’s Research (MJFF) and validated the approach to improve consistency in α-syn aggregation, neuroinflammation, and nigral neurodegeneration outcomes. The scientific significance is that it provides a reproducible, community-distributed experimental platform to strengthen comparability of α-syn overexpression studies.

Pardo J, Mudannayake J, Bernal-Conde LD et al. · Journal of Parkinson’s disease · (2026) · View on PubMed ↗ · Free PDF ↗

SEMI-1, A Novel Neuronal Selenium-Binding Protein 1 Homolog Without Methanethiol Oxidase Activity, Modulates Stress Resistance, Lifespan, and Thermotaxis in C. elegans.

The study characterized a novel Caenorhabditis elegans ortholog of human selenium-binding protein 1 (SELENBP1), named SEMI-1, focusing on its neuronal expression and function in stress resistance, lifespan, and thermotaxis. Unlike SELENBP1 and the previously described C. elegans ortholog SEMO-1, SEMI-1 is methanethiol oxidase (MTO) inactive and is expressed specifically in thermosensory AFD and oxygen-sensing BAG neurons using a SEMI-1::GFP reporter. Loss of SEMI-1 alters stress resistance and behavioral/aging phenotypes, indicating that SELENBP1-family proteins can modulate organismal physiology through MTO-independent mechanisms in defined sensory neurons.

Gong W, Köhnlein K, Priebs J et al. · BioFactors (Oxford, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Multiplexed perturbation enables scalable pooled screens.

This paper studied how multiplexing guide RNAs in pooled CRISPR interference screens affects performance and scalability. By evaluating co-delivery of multiple sgRNAs via high multiplicity of infection (MOI), the authors quantified impacts on knockdown efficiency, sgRNA representation, and screen reliability to reduce required cell numbers. The work provides a practical strategy for scalable pooled CRISPR screening using multiplexed perturbation.

Oberlin S, Tay NQ, Xue A et al. · Nature methods · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

Subcellular chemical mapping using correlated cryogenic electron and mass spectrometry imaging.

The study developed a correlative workflow for subcellular chemical mapping by combining cryogenic electron cryomicroscopy with chemical imaging. Using focused ion beam secondary ion mass spectrometry (FIB-SIMS) alongside cryo-EM, the authors achieved integrated spatiochemical localization of molecules in untagged bacterial cells and compatibility with cryogenic light microscopy and FIB-milled lamellae for eukaryotic specimens. As a demonstration, they investigated uptake of bisphenol-AF, showing that the method can chemically identify densities observed by cryo-EM at subcellular resolution.

Ochner H, Isbilir B, Blasche S et al. · Nature methods · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

A kinetics-based model of haematopoiesis reveals extrinsic regulation of skewed lineage output from stem cells.

This study created a kinetics-based model of haematopoiesis to explain how extrinsic regulation shapes skewed lineage output from murine hematopoietic stem cells (HSCs). Using single-cell transplantations of over 1,000 highly purified long-term HSCs with deep phenotyping of clonal progeny, the authors inferred reconstitution kinetics that aligned HSCs into a single hierarchical trajectory, showing that previously observed lineage biases are transitory states along a linear path rather than stable discrete conditions. The model links HSC heterogeneity to dynamic extrinsic control, improving mechanistic interpretation of lineage skewing in vivo.

Rodríguez-Correa E, Grünschläger F, Nizharadze T et al. · Nature cell biology · (2026) · View on PubMed ↗ · Free PDF ↗

Human amygdala-like telencephalic organoids model stress circuitry in assembloid systems.

Human amygdala-like telencephalic organoids (hATOs) were generated and assembled with hypothalamic organoids with paraventricular nucleus (PVN)-like features to model amygdala–hypothalamus-like stress circuitry in an ex vivo human system. The assembloid model recapitulated region-specific development and key features of amygdala-related stress circuitry, enabling functional modeling of stress responses. This provides a human organoid platform to study circuit mechanisms underlying anxiety/stress-related disorders and to test candidate interventions.

Yang WS, Choe MS, Lo C et al. · Cell stem cell · (2026) · View on PubMed ↗

Human retinal organoids functionally bridge a transected optic nerve in a rat model.

Human retinal organoids were heterotopically transplanted into the transection cavity of the optic nerve in adult rats to test whether they can restore vision after complete optic nerve injury. One month post-transplantation, treated rats showed partial functional recovery (direct pupillary light reflex, visually evoked electrophysiology, and visually guided behaviors) that persisted for at least 3 months, along with structured host–graft coupling across the gap. This demonstrates a translationally relevant strategy for bridging optic nerve transections using human retinal organoid tissue.

Gong Y, Zhu H, Ge L et al. · Cell stem cell · (2026) · View on PubMed ↗

The Landscape of Clinical Trials for TCR-T Cell Therapy.

This study systematically mapped the clinical trial landscape for T cell receptor-engineered T cell (TCR-T) therapy using the Trialtrove database (260 trials before April 1, 2026). It characterized trial phases, statuses, disease indications, primary targets, and investigational drugs to reveal trends in TCR-T development across solid and hematologic malignancies. The resulting overview helps guide researchers and clinicians toward the most active targets and indications for future TCR-T trials.

Fan X, Yu T, Liao Q et al. · American journal of clinical oncology · (2026) · View on PubMed ↗

Dose-Response of Dietary Carbohydrate Intake on Skeletal Muscle Glycogen, Gastrointestinal Comfort and Body Composition in Endurance-Trained Individuals in Simulated Preparation for Competition.

This counterbalanced repeated-measures study in 11 endurance-trained athletes (3 women, 8 men) tested different dietary carbohydrate (CHO) intakes during simulated pre-competition training to determine dose-response effects on skeletal muscle glycogen and related outcomes. Different CHO doses during the final 48 hours altered muscle glycogen concentration and influenced gastrointestinal comfort and body composition measures. The findings support evidence-based CHO dosing to maximize pre-race muscle glycogen while managing tolerability in athletes who continue training.

Jones RO, Areta JL, Bennett S et al. · Scandinavian journal of medicine & science in sports · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on May 27, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.