PubMed Trending Research Digest — June 12, 2026
A curated digest of 98 trending PubMed articles, automatically categorised and summarised across 15 research areas.
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PubMed Trending Research Digest — June 12, 2026
Automated digest · 98 articles · 15 research areas · June 12, 2026
Overview
This week’s research is dominated by two converging trends: (1) building mechanistic maps from high-dimensional biology (single-cell atlases, allele-specific expression, and multi-omics) and (2) translating those maps into more precise interventions—whether drugs, imaging-guided decisions, or programmable therapies.
Across neuro-oncology and neurodegeneration, studies used brain-wide connectivity frameworks, subtype/stage inference from multimodal imaging, and circuit-level experiments to explain how disease spreads or how behavior is computed. In parallel, multiple papers leveraged genomics and RNA biology—ranging from whole-genome duplication’s role in vertebrate cell-type evolution to structural cryo-EM insights into RISC assembly and programmable RNA editing strategies for DMD—highlighting how gene regulation and RNA processing can be both biomarkers and therapeutic levers.
On the translational side, several trials and preclinical studies emphasize “context-aware” treatment: iron-driven ferroptosis as a mechanism of CAR-T dysfunction, pulsatile FXR agonism to balance efficacy and safety, and PSMA PET-CT to reduce unnecessary prostate biopsies. Meanwhile, immunology and host–pathogen work (including microbiome/SCFA effects and pathogen-induced immune failure via defined molecular pathways) reinforce a broader theme: many diseases are shaped by specific microenvironmental constraints—metabolic, immune, or structural—so targeting the constraint can be more effective than applying blanket modulation.
Neuro-oncology & Brain Tumor Imaging/Prognosis
Helicopter emergency medical services for interfacility transfers: an Italian expert consensus.
This multicenter retrospective cohort study assessed neurological outcomes after out-of-hospital cardiac arrest (OHCA) due to aneurysmal subarachnoid hemorrhage (aSAH) in adults admitted alive to 12 French neuro-ICUs between 2014 and 2024. Using 6-month modified Rankin Scale (mRS) outcomes and Firth penalized logistic regression, the study aimed to identify predictors of favorable neurological outcome. The clinical significance is improved prognostication and risk stratification for a rare but devastating OHCA-aSAH presentation.
Accurso G, Carenzo L, Palmeri M et al. · Scandinavian journal of trauma, resuscitation and emergency medicine · (2026) · View on PubMed ↗ · Free PDF ↗
A prognostic human brain network for diffuse midline glioma.
The study developed a tumor network mapping approach to compute brain-wide connectivity profiles for diffuse midline glioma (DMG) in living humans. It reported a prognostic human brain network for DMG that reflects conserved brain-wide connectivity patterns relevant to tumor spread. This network framework could improve risk stratification and guide therapeutic targeting of the connectivity features that drive DMG lethality.
Sidpra J, Lind V, Cohen AL et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗
Drp1-driven fragmentation of scleral mitochondria promotes myopia development.
This study examined whether Drp1-driven mitochondrial fission and scleral mitochondrial fragmentation causally promote myopia development in mammalian animal models. The key finding was that increased mitochondrial fission (via Drp1) drives pathological scleral remodeling and myopia progression. These results suggest that targeting mitochondrial dynamics could be a therapeutic strategy to prevent or slow myopia progression.
Guan Z, Li W, Liu S et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
The autophagy protein ATG-9 promotes aversive learning in Caenorhabditis elegans through trafficking neuropeptide receptors.
This study used Caenorhabditis elegans to test how the autophagy transmembrane protein ATG-9 regulates aversive learning under mitochondrial stress, focusing on synaptic trafficking of neuropeptide receptors. The key finding was that mitochondrial stress upregulates synaptic ATG-9 through AP-1/AP-2–dependent exocytosis and endocytosis, and that disrupting autophagy genes including atg-9 impairs aversive learning. Scientifically, it links synaptic autophagy machinery to stress-responsive neural circuit plasticity via neuropeptide receptor trafficking.
Tam WH, Tang YC, Shiu HH et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗
Neurodegeneration & Brain Circuit Mechanisms
Receptor and cell-type-specific mechanisms in mesocortical dopamine circuits gate chronic pain and comorbid anxiodepression.
This study examined receptor- and cell-type-specific mechanisms in mesocortical dopamine circuits in a trigeminal neuralgia (TN) mouse model, focusing on orbitofrontal cortex (OFC) D1R- and D2R-expressing neurons and the ventral tegmental area (VTA)→OFC pathway. It found that OFC D1R- and D2R-expressing neurons independently gate anxiodepression and allodynia, and that activating the VTA→OFC circuit alleviated TN-induced allodynia and anxiodepressive-like behaviors, with effects abolished by selective blockade of D2Rs and D1Rs, respectively. These results identify dopamine receptor-specific circuit checkpoints that could guide targeted neuromodulation or pharmacotherapy for chronic pain with comorbid anxiety/depression.
Cai YQ, Hou XY, Wang GH et al. · Neuron · (2026) · View on PubMed ↗
Linking GWAS risk genes to transcriptional features of major depressive disorder via in vivo Perturb-seq.
This study linked genome-wide association study (GWAS) risk genes for major depressive disorder (MDD) to in vivo transcriptional effects by building an AAV-Perturb-seq system for parallel loss-of-function screening in mouse brain. Comparing perturbation signatures with patient MDD transcriptomes identified a cluster of risk genes whose loss downregulated neuronal oxytocin signaling, matching a shared patient feature, and mechanistic work highlighted Dennd1a as an example. This provides an in vivo functional map from MDD GWAS loci to specific neuronal gene-expression programs, prioritizing oxytocin-pathway biology for downstream therapeutic exploration.
Zhang L, Kong X, Ma Q et al. · Nature genetics · (2026) · View on PubMed ↗
A thalamus-brainstem attractor network drives history-biased decisions.
This study investigated how a thalamus–brainstem circuit implements history-biased (serial dependence) decision-making using whole-brain, cellular-resolution imaging in zebrafish performing memory-guided evasive maneuvers. It identified a hierarchical attractor network that maintains past information and biases future choices, providing a circuit-level mechanism for history-dependent decisions. The work advances mechanistic understanding of how neural circuits compute serial dependence, informing models of adaptive behavior and memory-guided control.
Zhao S, Shan H, Liu X et al. · Nature · (2026) · View on PubMed ↗
The 25-Year Evolution of Lithium as a Disease-Modifying Agent in Dementia: A Narrative Review.
This narrative review assessed the evidence for lithium as a disease-modifying agent in neurodegenerative disorders, focusing on mild cognitive impairment (MCI) and Alzheimer disease (AD). It highlighted multi-pathway mechanisms of chronic lithium exposure, including upregulation of the anti-apoptotic protein BCL-2, enhanced brain-derived neurotrophic factor (BDNF) signaling, inhibition of glycogen synthase kinase-3β (GSK-3β), mitochondrial stabilization, and reduced oxidative stress. The review’s significance is that it frames lithium as a pleiotropic, biologically plausible candidate for disease modification rather than single-target amyloid/tau approaches.
Moore GJ, Bose N, Henter ID et al. · JAMA psychiatry · (2026) · View on PubMed ↗
Targeted neuronal reprogramming rescues memory and neural synchrony in Alzheimer’s disease.
This study tested whether targeted, intermittent expression of Yamanaka factors (YFs) in hippocampal neurons can rescue Alzheimer disease phenotypes in the P301S mouse model of tauopathy. The key finding was that controlled YF expression restored memory and improved neural synchrony/network integrity, consistent with improved excitatory synaptic function. The significance is that it supports targeted neuronal reprogramming as a potential strategy to counteract tauopathy-associated cognitive and circuit dysfunction.
Galán-Ganga M, Rodríguez-Navarro I, Zaballa S et al. · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗
Mitochondrial Dysfunction as a Driver of Neurodegeneration in Parkinson’s and Huntington’s Disease: Molecular Insights and Emerging Interventions.
This review synthesizes evidence on how mitochondrial dysfunction drives neurodegeneration in Parkinson’s disease and Huntington’s disease, focusing on pathways involving PINK1 and Parkin mitochondrial quality control and mutant huntingtin effects on mitochondrial dynamics, transport, and ATP production. It highlights that α-synuclein aggregation in Parkinson’s and mutant huntingtin in Huntington’s converge on a shared pathological axis of impaired mitochondrial function that worsens neuronal vulnerability. Targeting mitochondrial quality control and bioenergetic/transport defects is presented as a promising emerging therapeutic strategy across both disorders.
Kuwar OK, Khan S, Maloo A et al. · Molecular neurobiology · (2026) · View on PubMed ↗
Identifing two distinct cortical progression subtypes of Parkinson’s disease through multimodal neuroimaging.
This cross-sectional multimodal neuroimaging study examined 317 clinically diagnosed Parkinson’s disease patients and 61 healthy controls using simultaneous FDG-PET and MRI, applying the SuStaIn (Subtype and Stage Inference) model to cortical glucose metabolism and thickness to infer latent progression patterns. It identified two distinct cortical progression subtypes with different trajectories of cortical involvement, further characterized using network-level analyses within a whole-brain gradient framework. These subtype-specific progression maps could improve patient stratification and prognostic modeling in Parkinson’s disease.
Yu Q, Guan X, Wu J et al. · European journal of nuclear medicine and molecular imaging · (2026) · View on PubMed ↗
Developmental circuit instability in amyotrophic lateral sclerosis: from hyperexcitability to network collapse.
This experimental study used cultured cortical networks derived from SOD1G93A mouse embryos and applied morphometric, electrophysiological, pharmacological, molecular, computational, and machine-learning approaches to model developmental circuit instability in amyotrophic lateral sclerosis (ALS). It found that ALS neurons fail to acquire mature polarization and connectivity, showing a transient hyperexcitability phase that precedes progressive network collapse, with astrocytic dysfunction emerging early. The significance is that it links early developmental-like network changes to ALS pathogenesis, identifying potential early intervention windows before irreversible collapse.
Donati Della Lunga I, Cerutti L, Barabino V et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗
Genomics, Epigenomics & Single-Cell Atlases
Allele specific expression in Alzheimer’s disease.
This study performed genome-wide allele-specific expression (ASE) profiling across seven brain regions in 2,231 Alzheimer’s disease (AD) and control donors from the Mount Sinai Brain Bank and ROSMAP, using single-cell analyses to assess cell-type-specific activity. The authors identified 56,136 ASE variants enriched in imprinted regions (e.g., chr6, chr14q32, chr15q11), including ASE within exons, suggesting parent-of-origin–linked dysregulation in AD. These findings support ASE and imprinting as mechanistic contributors to AD pathobiology and provide candidate loci for future functional validation.
Wang Z, Hossain D, Wang JJ et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗
Mutation-dependent responses to sleep and exercise in clonal haematopoiesis.
This study examined how lifestyle factors modify clonal haematopoiesis (CH) in humans and mice, testing mutation-dependent responses across Jak2, Tet2, Trp53, and Dnmt3a. It found that mutant CH cells respond uniquely to sleep and exercise, with moderate-to-vigorous physical activity associated with lower prevalence of non-DNMT3A-driven CH in human datasets, and in mice uninterrupted sleep reduced CH expansion specifically in Jak2V617F or Tet2 LOF models. The findings indicate that CH biology is mutation-specific and that lifestyle may differentially influence atherosclerosis risk depending on the underlying CH driver mutation.
Gerhardt T, Jacob W, Gaebel L et al. · Nature · (2026) · View on PubMed ↗
Whole-genome duplication shaped cell-type evolution in the vertebrate brain.
The study used brain single-cell transcriptomes from five chordates (human, mouse, lizard, lamprey, and amphioxus) to test how whole-genome duplication (WGD) shaped vertebrate cell-type evolution. It found that many vertebrate cell-type families with conserved core transcription factors do not show one-to-one homology with amphioxus, and that ohnologues—especially from the first WGD—contributed more to vertebrate cell-type evolution than small-scale duplication paralogues. This supports a model in which early WGD provided dosage and regulatory diversification that enabled expansion and specialization of vertebrate brain cell types.
Zhu Y, Zhang S, Wei J et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗
SIRT7 regulates dosage compensation and safeguards the female X chromosome.
The study examined sex differences in mice using Sirt7 knockout (Sirt7-/-) to determine how SIRT7 affects dosage compensation and female X-chromosome regulation. It found that SIRT7 preferentially localizes to sex chromosomes and that SIRT7 loss in females disrupts X-chromosome inactivation, with Xist overexpression and altered silencing efficiency, leading to decreased female fitness across the lifespan. These findings identify SIRT7 as a regulator of X-inactivation and suggest a mechanistic basis for sex-specific vulnerability in mammalian disease.
Simonet NG, Thackray JK, Kesner B et al. · Nature · (2026) · View on PubMed ↗
Cerebrovascular vulnerability and fibrosis in human brain aneurysms.
The study profiled 227,663 neurovascular cells, including 52,946 aneurysmal cells, from 14 adult human brain aneurysms and 11 controls using cell-resolution spatial transcriptomics. It found that aneurysm remodeling involves loss of structurally supportive smooth muscle cells and emergence of activated perivascular fibroblasts expressing multiple aneurysm-risk genes, linking fibrosis-like changes to aneurysm pathology. This atlas-level evidence identifies cell types and gene programs that may underlie aneurysm formation and rupture, informing future biomarkers and interventions.
Wang JC, Kim CN, Bhalla S et al. · Nature neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗
Hetairos is a histology-based artificial intelligence model for predicting central nervous system tumor methylation subtypes.
The study introduced Hetairos, a histology-based AI model that predicts 102 CNS tumor methylation subtypes from digital H&E slides, and validated it across 11 centers. It found that Hetairos achieved accuracy of 0.87 for its highest-rated predictions and identified 50–70% of cases with high confidence using training/validation data from 9,606 patients and over 11,000 slides. This could reduce reliance on resource-intensive methylation profiling by enabling scalable, histology-only subtype prediction for CNS tumors.
Jin D, Shmatko A, Patel A et al. · Nature cancer · (2026) · View on PubMed ↗ · Free PDF ↗
Unraveling the HGF/MET axis in Mallory-Denk body pathogenesis associated with liver fibrosis through single-cell transcriptomics.
This single-nucleus RNA sequencing (snRNA-seq) study investigated the cellular interactions underlying Mallory-Denk body (MDB) pathogenesis in liver fibrosis, focusing on the HGF/MET axis and defining disease-associated hepatocyte and hepatic stellate cell (HSC) states. It identified an MDB-associated hepatocyte (MAH) subpopulation and a unique activated HSC (aHSC) subtype correlated with hepatocellular carcinoma progression, revealing a tightly connected MAH–aHSC signaling axis consistent with HGF/MET involvement. The findings provide mechanistic targets for interrupting MDB-associated fibrogenic crosstalk and potentially modulating progression toward HCC.
Tang X, Shi Y, Pan J et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗
IBDome: An integrated molecular, histopathological, and clinical atlas of inflammatory bowel diseases.
This multi-cohort atlas study analyzed 1,002 clinically annotated inflammatory bowel disease (IBD) patients and non-IBD controls using whole-exome and RNA sequencing of normal and inflamed gut tissues, serum proteomics, and histopathology from H&E images. It found distinct transcriptomic patterns between normal and inflamed tissues with site-specific inflammatory signatures across IBD contexts. The resulting IBDome resource is significant for improving IBD diagnostics and enabling more personalized therapeutic strategies through integrated molecular and clinical stratification.
Plattner C, Sturm G, Kühl AA et al. · Gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗
International Union of Basic and Clinical Pharmacology. CXXII. Applying an objective evaluation to the status of class A orphan G protein-coupled receptors.
This IUPHAR (International Union of Basic and Clinical Pharmacology) review assessed objective criteria for deorphanizing class A G protein-coupled receptors (GPCRs) by pairing orphan receptors with endogenous/physiological ligands. Applying these standards to 67 orphan class A GPCRs, the review highlights which receptors lack identified endogenous agonists and illustrates the evidence framework using specific examples including GPR21, GPR27, GPR52, GPR85, and GPR88. The work is significant because it standardizes how receptor–ligand evidence is evaluated, accelerating more rigorous and reproducible GPCR deorphanization.
Alexander SPH, Bennett KA, Brown AJ et al. · Pharmacological reviews · (2026) · View on PubMed ↗ · Free PDF ↗
Oligogenic variants in NEK1 and ATXN2 in amyotrophic lateral sclerosis: report of two cases and review of the literature.
This report described two siblings with amyotrophic lateral sclerosis (ALS) carrying an ATXN2 heterozygous 32-CAG trinucleotide repeat expansion and a novel NEK1 heterozygous c.1674_1677dup variant, with segregation assessed across a large family. The co-segregation of both oligogenic variants in the family supported a potential combined contribution of ATXN2 and NEK1 to ALS risk beyond single-gene causality. Clinically, the findings strengthen the rationale for considering oligogenic variant models (ATXN2/NEK1) in ALS genetic workups when penetrance is incomplete.
Roy É, Blais M, Dion P et al. · Amyotrophic lateral sclerosis & frontotemporal degeneration · (2026) · View on PubMed ↗
Changes in Genetic Contributions to ASD and ADHD by Year of Diagnosis.
This cohort study analyzed changes in genetic contributions to autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) by year of diagnosis using data from the Norwegian population registry (Lun [truncated]). It found that the genetic risk profile of individuals diagnosed with ASD or ADHD varied by diagnosis year compared with expectations under simulated scenarios. The significance is that it tests whether rising ASD/ADHD incidence reflects shifts in underlying genetic risk rather than only diagnostic practice or awareness.
LaBianca S, Lousdal ML, Dybdahl Krebs M et al. · JAMA psychiatry · (2026) · View on PubMed ↗
Gene Regulation, RNA Biology & RNA Editing
Structural basis for chaperone-guided assembly of RNA-induced silencing complex.
The study investigated human RNA-induced silencing complex (RISC) assembly by identifying the AGO maturation complex (AMC) containing Argonaute (AGO) with HSP90 and p23, and then determining its structure by cryogenic electron microscopy (cryo-EM) with a microRNA duplex. It found that the AGO-HSP90-p23 AMC captures AGO in an RNA-free, open state that enables RNA loading and AGO folding, and that the AMC–microRNA duplex structure differs from AGO’s conformation in mature RISC. This provides a structural mechanism for chaperone-guided small RNA loading onto AGO, clarifying how de novo RISC assembly is initiated.
Lee YY, Jeong M, Lee H et al. · Nature · (2026) · View on PubMed ↗
RNA structure programs endogenous ADAR for precise and efficient editing.
This mechanistic study investigated how cisplatin triggers neuronal death, focusing on DNA repair pathways in post-mitotic neurons. It found that nucleotide excision repair (NER) removes cisplatin lesions but paradoxically promotes neuronal death due to low neuronal dNTP pools, where transcription-coupled NER consumes dNTPs and leads to repair failure. Scientifically, it identifies a repair–metabolism vulnerability that could inform strategies to prevent cisplatin neurotoxicity.
Song D, Liu G, Zhang W et al. · Cell · (2026) · View on PubMed ↗
Continuous modeling of primate embryogenesis from totipotency to early organogenesis.
This translational study used LEAPER 2.0, an ADAR-based RNA editing platform with circular ADAR-recruiting RNAs (circ-arRNAs), to induce exon skipping in the DMD gene in DMD nonhuman primates and humans. It found that a single administration of circ-arRNA-guided exon skipping restored dystrophin expression and enabled long-term reversal of Duchenne muscular dystrophy phenotypes in monkeys and humans. Clinically, it supports a potentially durable, mutation-targeted RNA editing approach for DMD.
Zheng W, Peng B, Chen Z et al. · Cell · (2026) · View on PubMed ↗
Long-term reversal of Duchenne muscular dystrophy via circular arRNA-guided exon skipping in monkeys and humans.
This study examined how LEAPER 3.0 improves endogenous ADAR-driven RNA editing by using RNA structure to program ADAR recruitment and editing outcomes. It found that integrating AlphaFold 3 structural predictions with biochemical and cellular assays defined the ADAR1/ADAR2–double-stranded RNA interface, enabling rational optimization of arRNAs for higher precision and efficiency. Scientifically, it advances a design framework for programmable, exogenous-enzyme-free RNA editing with improved performance.
Guo W, Tang H, Yi Z et al. · Cell · (2026) · View on PubMed ↗
Immunology & Tumor Microenvironment
Immune microenvironment and noncoding RNA shape early colorectal carcinogenesis in patients with premalignant lesions.
This study performed multimodal profiling of the immune microenvironment across 258 longitudinal premalignant colorectal lesions from 26 patients to determine how immune states and noncoding RNA programs relate to early carcinogenesis and polyp development rate. The key finding was that distinct immune states were associated with polyp burden and that noncoding RNA features helped shape these immune dynamics during the premalignant phase. Scientifically, it identifies immune–noncoding RNA coupling as a driver of early colorectal tumorigenesis and suggests potential biomarkers for risk stratification and early intervention.
Morgand E, Van den Eynde M, Nguyen H et al. · Science translational medicine · (2026) · View on PubMed ↗
Smoothened and ciliary GPCRs regulate ciliary protein kinase A activity involved in Hedgehog signal transduction.
This mechanistic study investigated how Smoothened (SMO) and ciliary GPCRs regulate ciliary protein kinase A (PKA) activity to control Hedgehog (HH) signal transduction in zebrafish, using a ciliary PKA reporter. The key finding was that HH pathway activation by Sonic hedgehog (SHH) or a SMO agonist (SAG) inhibited ciliary PKA, linking SMO-dependent signaling to PKA suppression at the primary cilium. This advances the scientific understanding of how ciliary GPCR/SMO signaling gates transcriptional GLI output by modulating local kinase activity.
Nguyen TD, Konjikusic MJ, Del Castillo LM et al. · PLoS biology · (2026) · View on PubMed ↗ · Free PDF ↗
Peptide-MHC-targeted engineered virus-like particles enable selective priming and gene editing of tumor-specific T cells.
This study developed peptide–MHC–targeted engineered virus-like particles (eVLPs) to selectively prime and genome-edit tumor-specific CD8+ T cells within a patient’s endogenous TIL repertoire. The key finding was that pMHC-pseudotyped eVLPs enabled coordinated priming, expansion, and genome editing of rare antigen-specific CD8+ T cells more selectively than non-targeted approaches. Clinically, it provides a programmable platform to improve the efficacy of TIL-based therapies by reprogramming low-frequency tumor-specific clonotypes.
Shim BH, Zhao QH, Queenan JA et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer Therapeutics (Drugs, Trials, and Outcomes)
High-Dose Methotrexate as CNS Prophylaxis in Ultra High-Risk Large B-Cell Lymphoma: An International Multicenter Analysis.
This international multicenter analysis studied the impact of high-dose methotrexate (HD-MTX) as CNS prophylaxis specifically in ultra high-risk (UHR) patients with large B-cell lymphoma (LBCL). By combining data from two prior retrospective analyses, it compared outcomes in UHR patients treated with versus without HD-MTX using UHR criteria such as CNS-IPI 5–6 and specific high-risk extranodal sites. The study aims to resolve uncertainty in guideline recommendations by providing subgroup-specific evidence for whether HD-MTX improves CNS relapse prevention in UHR LBCL.
Wilson MR, Lewis KL, Kirkwood AA et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Donanemab treatment effect by baseline tau burden and disease severity: Observations from the TRAILBLAZER-ALZ 2 trial.
This analysis evaluated the clinical effect of donanemab on CDR-SB in participants from the TRAILBLAZER-ALZ 2 trial, stratifying by baseline tau PET, plasma P-tau217, and predicted disease progression stage. Donanemab slowed disease progression across both baseline tau PET and plasma P-tau217 strata, with greater slowing in participants who had lower baseline tau PET and P-tau217 versus placebo. Clinically, this supports earlier treatment initiation and tau/P-tau217–informed patient selection for maximizing benefit from anti-amyloid/anti-tau–targeted disease modification.
Raket LL, Lu M, Evans CD et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗
Chinese expert consensus on conversion and perioperative therapy of primary liver cancer (2024 edition).
This 2024 Chinese expert consensus (updated for clinical use) synthesized evidence to standardize conversion and perioperative therapy strategies for primary liver cancer in China, addressing intermediate-to-advanced disease where curative surgery is often not feasible. It provides structured recommendations integrating systemic immunotherapy combinations (immune checkpoint inhibitor–based regimens) and locoregional therapies to improve eligibility for surgery and reduce recurrence risk. The consensus is significant for harmonizing real-world treatment pathways and guiding multidisciplinary decision-making in perioperative liver cancer care.
Wang Z, Sun H, Zhou J et al. · Hepatobiliary surgery and nutrition · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
The All-Oral Combination of Revumenib, Decitabine and Venetoclax for Relapsed or Refractory Acute Myeloid Leukemia (SAVE).
This phase 1–2 clinical trial evaluated an all-oral regimen combining revumenib (a menin–KMT2A inhibitor), decitabine/cedazuridine, and venetoclax in patients aged ≥12 years with relapsed or refractory acute myeloid leukemia (AML). The study targeted AML subtypes defined by KMT2A rearrangement (KMT2Ar), NPM1 mutation (NPM1mt), or NUP98 rearrangement (NUP98r), with dosing of decitabine/cedazuridine on days 1–5, venetoclax on days 1–14, and revumenib on days 1–28. The trial’s significance lies in testing a rational, menin–KMT2A–directed strategy plus BCL2 inhibition for improved outcomes in genetically defined R/R AML.
Issa GC, Cuglievan B, El Hajjar G et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Molecular glue degraders of HuR suppress BRAF-mutant colorectal cancer.
This study used rational chemical library design and parallel proteomic screening to identify dHuR, a molecular glue degrader of the RNA-binding protein HuR (human antigen R), as a therapy for BRAF-mutant colorectal cancer. dHuR suppressed HuR function and inhibited growth of BRAF-mutant CRC models, addressing resistance mechanisms associated with BRAF(V600E) and MAPK pathway reactivation. The results position HuR degradation as a potential strategy to improve outcomes in CRC patients with limited options beyond BRAF/EGFR combination approaches.
Lu X, Wang X, Yang Z et al. · Nature · (2026) · View on PubMed ↗ · Free PDF ↗
Iron-mediated ferroptosis impairs CAR-T cell function and antitumor efficacy.
The study combined integrated analyses of clinical samples from multiple myeloma and acute lymphoblastic leukemia patients treated with CAR-T cells with preclinical and ex vivo experiments to test how iron affects CAR-T function. It found that after rapid CAR-T expansion there is a diminution phase with ferroptosis-associated features and elevated serum iron, and that excess intracellular iron impairs CAR-T function by promoting ferroptosis. This identifies iron-driven ferroptosis as a mechanism of CAR-T dysfunction and suggests that iron/ferroptosis modulation could improve durability of CAR-T therapy.
Kong D, Yang T, Zhao M et al. · Nature cancer · (2026) · View on PubMed ↗
Trial design and end points in hepatocellular carcinoma: an EASL-AASLD-ILCA consensus statement.
This consensus statement reviewed and harmonized trial design and endpoints for hepatocellular carcinoma (HCC) across evolving treatment settings, including immunotherapy-dominated advanced disease and perioperative/intermediate-stage trials. It emphasized that discrepancies between positive phase III results and subsequent guideline/regulatory adoption highlight the need to update standards for endpoints and trial design. Scientifically, it provides a framework to improve comparability and interpretability of HCC clinical trials as new therapies and trial contexts expand.
Llovet JM, Mauro E, Rimassa L et al. · Nature reviews. Clinical oncology · (2026) · View on PubMed ↗
The future is not always uniform: rethinking radiotherapy through spatial fractionation.
This review studied how radiotherapy can be redesigned for large, bulky, or anatomically complex tumors where uniform dose escalation is limited by normal-tissue tolerances, focusing on spatially fractionated radiotherapy (SFRT). It found that SFRT intentionally creates intratumoural dose heterogeneity using high-dose “peaks” and low-dose “valleys” as an alternative to uniform target irradiation. Clinically, this reframes treatment planning toward exploiting controlled heterogeneity to improve local control while respecting organ-at-risk constraints.
Iori F, Tubin S, Mourad WF et al. · Nature reviews. Clinical oncology · (2026) · View on PubMed ↗
Effect of [68Ga]Ga-PSMA-11 PET-CT in the diagnosis of prostate cancer in men with equivocal or clinically high-risk non-suspicious findings on multiparametric MRI (PRIMARY2): a multicentre, non-inferiority, phase 3, randomised controlled trial.
This multicentre, non-inferiority phase 3 randomized controlled trial studied whether [68Ga]Ga-PSMA-11 PET-CT can reduce prostate biopsy in men with equivocal or clinically high-risk but non-suspicious findings on multiparametric MRI (PRIMARY2). It found that PSMA PET-CT could limit biopsy to targeted cores and reduce the number of men requiring biopsy without compromising the diagnosis of clinically significant prostate cancer. The trial is significant because it supports PSMA PET-CT as a decision tool to improve biopsy efficiency and reduce unnecessary sampling in MRI-negative/high-risk patients.
Buteau JP, Moon D, Fahey MT et al. · The Lancet. Oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Glofitamab plus gemcitabine and oxaliplatin for relapsed/refractory DLBCL: 3-year follow-up of STARGLO.
This report provided 3-year follow-up results from the phase 3 STARGLO trial evaluating glofitamab plus gemcitabine and oxaliplatin (Glofit-GemOx) versus rituximab plus gemcitabine and oxaliplatin (R-GemOx) in relapsed/refractory diffuse large B-cell lymphoma (DLBCL) patients ineligible for autologous stem cell transplant. With a median overall survival follow-up of 35.1 months, Glofit-GemOx continued to show superior overall survival (median 25.5 vs 12.5 months; HR 0.60) and favorable progression-free survival compared with R-GemOx. These extended data support durable benefit of the CD20xCD3 bispecific antibody glofitamab-based regimen in this high-risk DLBCL population.
Abramson JS, Townsend W, Fox CP et al. · Blood advances · (2026) · View on PubMed ↗ · Free PDF ↗
Clinical validation of an HPV whole-genome sequencing assay for MRD detection in patients with HPV+ head and neck cancer treated with surgery.
This prospective clinical study evaluated an HPV whole-genome sequencing assay (HPV-DeepSeek) for minimal residual disease (MRD) detection in 103 patients with stage I–IV HPV+ head and neck cancer treated with surgery. The key finding was that HPV-DeepSeek provided prognostic MRD information after surgery and outperformed or compared favorably with existing circulating HPV DNA approaches and clinical standards for risk stratification. Clinically, this supports whole-genome sequencing–based HPV MRD testing to guide adjuvant therapy decisions in HPV+ head and neck cancer.
Hirayama S, Al-Inaya Y, Bryan ME et al. · Science translational medicine · (2026) · View on PubMed ↗
A phase II clinical trial of albumin-bound paclitaxel, cisplatin, gemcitabine (NABPLAGEM) and paricalcitol as neoadjuvant therapy in pancreatic cancer.
This phase II clinical trial evaluated neoadjuvant albumin-bound paclitaxel (nab-paclitaxel) plus cisplatin plus gemcitabine (NABPLAGEM) combined with the vitamin D receptor agonist paricalcitol in adults with stage I–III pancreatic ductal adenocarcinoma (PDAC) (NCT03138720). The key finding was the trial’s assessment of efficacy and safety for this VDR-targeted neoadjuvant regimen in previously untreated patients, including outcomes in relation to CA 19-9–enriched disease. If effective and tolerable, this strategy could improve perioperative management of PDAC by enhancing chemotherapy benefit through VDR activation.
Viniotis AF, Jameson GS, Wertheim BC et al. · The oncologist · (2026) · View on PubMed ↗ · Free PDF ↗
Artificially Sweetened and Sugar-Sweetened Beverage Intake and Risk of Liver Cancer.
This pooled analysis of 11 prospective cohort studies examined whether intake of artificially sweetened beverages (ASBs) and sugar-sweetened beverages (SSBs) is associated with incident liver cancer overall and by subtype (hepatocellular carcinoma [HCC] and intrahepatic cholangiocarcinoma [ICC]). The key finding was the reported association pattern between beverage type and liver cancer risk by subtype in prospective data. If confirmed, the results have public-health significance by clarifying whether ASBs or SSBs differentially influence liver carcinogenesis risk.
Watling CZ, Zhao L, Zhang X et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗
Preoperative chemotherapy with docetaxel, oxaliplatin, and S-1 for gastric cancer with extensive lymph node metastasis: 3-year follow-up results from JCOG1704.
This phase II trial evaluated preoperative chemotherapy with docetaxel, oxaliplatin, and S-1 (DOS) in patients with marginally resectable gastric cancer with extensive lymph node metastasis (ELM), focusing on HER2-negative disease and bulky nodal and/or para-aortic node metastasis, with 3-year follow-up outcomes from JCOG1704. The key finding was the reported 3-year survival performance of DOS after R0 resection compared with historical benchmarks from prior cisplatin plus S-1 strategies. Clinically, the results help define whether DOS can improve long-term outcomes for patients with ELM gastric cancer undergoing curative-intent surgery.
Kurokawa Y, Doki Y, Mizusawa J et al. · Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · (2026) · View on PubMed ↗ · Free PDF ↗
Quality-of-life assessment in the randomized JBCRG-M06/EMERALD study of eribulin plus dual HER2 blockade in HER2-positive locally advanced or metastatic breast cancer.
This quality-of-life analysis from the randomized JBCRG-M06/EMERALD trial compared eribulin versus a taxane, each combined with dual HER2 blockade (trastuzumab and pertuzumab), in HER2-positive locally advanced or metastatic breast cancer. Using EORTC QLQ-C30 v3.0, it assessed the extent and timing of QoL deterioration, particularly taxane-associated declines in global health status and related domains. The significance is that it determines whether an eribulin-based regimen can preserve patient-reported outcomes while maintaining anti-HER2 efficacy.
Iwatani T, Masuda N, Saji S et al. · Breast cancer (Tokyo, Japan) · (2026) · View on PubMed ↗
Molecular and clinical characteristics of patients with non-small cell lung cancer (NSCLC) harboring KRAS Q61 mutations to assess therapeutic responses.
This study analyzed diagnostic samples from 2011–2023 using next-generation sequencing (NGS) to characterize molecular and clinical features of non-small cell lung cancer (NSCLC) patients with KRAS Q61 mutations and assess therapeutic responses. Among 8862 analyzed probes, 487 patients (5.5%) had KRAS Q61 mutations and 365 were further analyzed, with most mutations being Q61H (74.0%) and Q61L (20.8%). The results are significant for defining the heterogeneity of KRAS Q61–mutant NSCLC and informing treatment-response expectations by molecular subgroup.
Ruge L, John F, Verheyen M et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗
TQB2618 plus penpulimab, alone or in combination with chemotherapy, for recurrent or metastatic nasopharyngeal carcinoma: a multicentre, two-cohort, phase 2 trial.
This phase 2, multicentre two-cohort trial evaluated dual immunotherapy targeting TIM-3 and PD-1 using TQB2618 plus penpulimab in recurrent or metastatic nasopharyngeal carcinoma, including a cohort with progression after prior PD-(L)1 blockade and a treatment-naïve cohort. The study design tests TQB2618 plus penpulimab every 3 weeks in the post–PD-(L)1 cohort and combines TQB2618, penpulimab, gemcitabine, and cisplatin followed by maintenance dual immunotherapy in the treatment-naïve cohort. The clinical significance lies in determining safety and objective response/progression-free survival potential for TIM-3/PD-1 blockade strategies in this patient population.
Xu C, Wang SY, Nie M et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗ · Free PDF ↗
Cardiovascular Critical Care & Resuscitation
Vasopressors or Fluids in Early Septic Shock.
This randomized clinical trial studied early resuscitation strategies in adult septic shock patients by comparing restricted-volume intravenous fluids plus early vasopressor therapy versus higher-volume fluids with later vasopressor therapy. The key finding (as assessed by the primary endpoint of days alive and out of the hospital) was intended to determine whether early vasopressor use with less fluid improves outcomes compared with fluid-heavy resuscitation. The results are significant for establishing evidence-based protocols that balance perfusion restoration against harms from excess fluid in early septic shock management.
Peake SL, Macdonald SPJ, Howe BD et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Sodium Bicarbonate for In-Hospital Cardiac Arrest: A Randomized Clinical Trial.
This randomized, parallel-group, double-blind, placebo-controlled trial studied whether administering sodium bicarbonate during in-hospital cardiac arrest improves return of spontaneous circulation (ROSC) in adults receiving at least one dose of epinephrine. The key finding tested whether bicarbonate increased the proportion of patients achieving ROSC compared with placebo. If effective, this would directly inform resuscitation medication practice during in-hospital cardiac arrest, where bicarbonate is commonly used despite uncertain benefit.
Granfeldt A, Kirkegaard BL, Vallentin MF et al. · JAMA · (2026) · View on PubMed ↗
Antidotes for Anticoagulation Reversal.
This narrative review summarized pharmacologic antidotes for anticoagulation reversal, focusing on how reversal choices depend on anticoagulant pharmacokinetics/pharmacodynamics and patient-specific factors. It highlights that protamine sulfate reverses unfractionated heparin, four-factor prothrombin complex concentrates reverse vitamin K antagonists, idarucizumab reverses dabigatran (with attention to possible rebound), and that no specific antidotes exist for low-molecular-weight heparins or fondaparinux. Clinically, the review supports faster, evidence-informed selection of reversal agents during major bleeding events.
Rocca B, Ten Cate H · The New England journal of medicine · (2026) · View on PubMed ↗
High-Dose Intravenous Vitamin C and Mortality and Organ Dysfunction in Severe Burn Injury: The VICTORY Randomized Clinical Trial.
This phase 3 randomized, double-blind, placebo-controlled trial studied high-dose intravenous vitamin C in adults (≥18 years) with deep second- and/or third-degree burns covering ≥20% total body surface area requiring skin grafting across 24 burn centers in North/Central/South America, Europe, and Asia. High-dose IV vitamin C did not reduce mortality or organ dysfunction compared with placebo. These results provide high-level evidence against routine use of high-dose IV vitamin C to improve outcomes after severe burn injury.
Stoppe C, Hill A, Cancio LC et al. · JAMA · (2026) · View on PubMed ↗
Conservative Oxygen for Unresponsive Patients after Cardiac Arrest.
This randomized trial studied conservative versus liberal oxygen therapy in unresponsive adults after cardiac arrest who were receiving mechanical ventilation in the ICU. Conservative oxygen targeted a pulse-oximetry SpO2 upper alarm of 95% with FiO2 reduced to 0.21 as needed, aiming to limit oxygen exposure beyond what was required for acceptable oxygenation. The study tests whether oxygen restriction improves survival with favorable functional outcome in post–cardiac arrest patients.
Hodgson CL, Mackle D, Mather AM et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Carbocisteine or Hypertonic Saline for Acute Respiratory Failure.
This multicenter, open-label, randomized 2-by-2 factorial trial studied carbocisteine (750 mg three times daily enterally) versus 6% or 7% nebulized hypertonic saline (4 mL four times daily) versus usual care alone in critically ill, mechanically ventilated patients (≥16 years) with acute respiratory failure and difficult-to-clear secretions. The trial evaluated whether these mucoactive agents reduce the duration of mechanical ventilation over up to 28 days. The results address a common ICU practice where evidence for effectiveness and safety has been limited.
Connolly B, Dickson N, Campbell C et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Hospital Policy of Tranexamic Acid to Reduce Transfusion in Major Noncardiac Surgery.
This multicenter, double-blind, cluster-randomized, placebo-controlled trial studied a hospital-wide policy of intraoperative tranexamic acid to reduce red-cell transfusion in patients undergoing major noncardiac surgery who were at high risk for transfusion. Hospitals were randomized at 4-week intervals to tranexamic acid policy versus placebo, with coprimary outcomes including red-cell transfusion during the index hospitalization and venous thromboembolism within 90 days. The study provides evidence on whether system-level tranexamic acid implementation safely reduces transfusion needs in major noncardiac surgery.
Houston BL, McIsaac DI, Breau RH et al. · The New England journal of medicine · (2026) · 1 citations · View on PubMed ↗
Cardiovascular Disease Risk, Epidemiology & Prevention
Neurological outcomes after out-of-hospital cardiac arrest due to aneurysmal subarachnoid hemorrhage: a multicenter cohort study.
This prospective study examined whether the C-reactive protein–triglyceride–glucose (CTI) index and central-obesity–modified CTI derivatives predict incident cardiometabolic multimorbidity (CMM) in middle-aged and older adults. Across two cohorts in China (CHARLS; n=6,498) and England (ELSA; n=2,455), participants free of diabetes, heart disease, and stroke at baseline were followed, with incident CMM defined as developing at least two cardiometabolic diseases. The significance is that CTI-related measures may help identify individuals at higher risk for developing multiple cardiometabolic conditions, especially in the context of central obesity.
Legros V, Darty F, Cateura J et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗
Association between lifestyle and risk of early-onset cancer: Evidence from the European Prospective Investigation into Cancer and Nutrition and the UK Biobank.
This study analyzed lifestyle factors and risk of early-onset cancers (EOCs; diagnosed before age 50) in participants from EPIC and the UK Biobank, stratifying by smoking, alcohol, BMI, physical activity, and diet. It evaluated associations between these modifiable exposures and EOC risk across multiple cancer sites (including breast, lung, colorectal, stomach, liver, cervix, esophagus, and bladder). The findings are intended to clarify which lifestyle changes could reduce the rising burden of early-onset cancers and guide prevention strategies.
Sala I, Botteri E, Berstad P et al. · European journal of cancer (Oxford, England : 1990) · (2026) · View on PubMed ↗
Global burden of non-communicable diseases attributable to ambient fine particulate matter pollution in adults aged 65 years and older from 1990 to 2021.
This global epidemiologic analysis used the Global Burden of Disease (GBD) 2021 dataset to estimate the NCD burden attributable to ambient fine particulate matter (PM2.5) among adults aged ≥65 years from 1990–2021 and forecast to 2031. The key finding was the quantified scale and temporal trends of PM2.5-attributable NCD deaths and disability-adjusted life years (DALYs), with trend metrics (EAPC) and Bayesian APC modeling used for projections. Public-health significance lies in identifying the magnitude and trajectory of PM2.5-related NCD harm in older adults to inform prevention and policy.
Zheng Z, Hairong Z, Xie W et al. · QJM : monthly journal of the Association of Physicians · (2026) · View on PubMed ↗
Outcomes of Cardiovascular Surgery in Patients With Multiple Sclerosis.
This cross-sectional nationwide study evaluated US inpatient outcomes of cardiovascular surgery (coronary artery bypass grafting, valve, aortic, or combined procedures) in patients with multiple sclerosis (MS) using the National Inpatient Sample from 2016 to 2022. The study aimed to quantify morbidity and mortality differences associated with MS in the perioperative setting, motivated by MS-related autonomic dysregulation and hemodynamic instability. Scientifically and clinically, the results address a major evidence gap by providing population-level estimates of surgical risk in MS patients undergoing cardiac procedures.
Diz Ferre JL, Zhou G, Cabulong A et al. · JAMA surgery · (2026) · View on PubMed ↗
Two Years of Menaquinone-7 Supplementation and Coronary Artery Calcification: A Randomized Clinical Trial.
This randomized placebo-controlled clinical trial tested whether 2 years of menaquinone-7 (MK-7), a vitamin K homologue, attenuates progression of coronary artery calcification (CAC) in symptomatic patients with coronary artery disease (CAC score 50–400 Agatston units) using the VitaK-CAC study design. The key finding was the trial’s effect of MK-7 supplementation versus placebo on CAC progression over 2 years. Clinically, the results inform whether vitamin K–based therapy can slow vascular calcification in established atherosclerotic CAD.
Vossen LM, de Leeuw PW, Schurgers LJ et al. · JAMA cardiology · (2026) · View on PubMed ↗
Diagnostic and prognostic accuracy of Berg Balance Scale and Mini-Balance Evaluation Systems Test in individuals with stroke: A systematic review and meta-analysis.
This systematic review and meta-analysis evaluated diagnostic and prognostic accuracy of the Berg Balance Scale (BBS) and Mini-BESTest cutoff values in individuals with stroke, using studies published through December 24, 2025. It aimed to determine which cutoff thresholds best match specific reference standards for predicting outcomes and balance-related impairment. The findings are clinically significant because they can standardize how BBS and Mini-BESTest are interpreted for stroke rehabilitation decision-making.
Kobayashi S, Kamo T, Ogihara H et al. · Physiotherapy theory and practice · (2026) · View on PubMed ↗
Heart Failure Duration, Cardiac Remodeling, Dysfunction, and Hemodynamic Severity in HFpEF and HFmrEF: Insights From REDUCE LAP-HF II.
This analysis of the REDUCE LAP-HF II trial (N=626) investigated how heart failure duration influences cardiac remodeling, dysfunction, hemodynamic severity, risk of worsening HF, and treatment response in HFpEF and HFmrEF patients (LVEF ≥40% with elevated exercise pulmonary capillary wedge pressure). It evaluated baseline structure/function and hemodynamics and related them to outcomes after randomization across different durations of HF diagnosis. The study is significant because it may clarify whether HF duration reflects distinct phenotypes/stages that affect prognosis and therapeutic benefit.
Doi S, Kazui S, Akashi N et al. · JACC. Heart failure · (2026) · View on PubMed ↗
Angiographic Quantitative Flow Ratio-Guided Coronary Intervention: 5-Year Follow-Up From the FAVOR III China Randomized Trial.
This report provides 5-year follow-up from the FAVOR III China randomized sham-controlled trial comparing quantitative flow ratio (QFR)–guided versus angiography-guided percutaneous coronary intervention (PCI) in coronary artery disease. It tests whether the earlier improvements in outcomes with QFR guidance persist long-term and evaluates long-term safety through extended follow-up. The significance is that it informs durability of benefit and risk tradeoffs for QFR-guided PCI strategies in routine clinical practice.
Zhang H, Guan C, Jin Z et al. · Journal of the American College of Cardiology · (2026) · 1 citations · View on PubMed ↗
Cardiovascular Disease Subtypes and Alzheimer’s Disease: Phenotypic and Genetic Associations in the UK Biobank and All of Us Research Program.
This cross-sectional genetic epidemiology study assessed associations between Alzheimer’s disease (AD) and 11 cardiovascular disease (CVD) subtypes using logistic regression in UK Biobank (n=502,133) and the All of Us Research Program (n=287,011). It also explored genetic overlap between AD and CVD traits, adjusting for demographic, lifestyle, and clinical covariates. The findings aim to refine which CVD phenotypes and shared genetic factors are most strongly linked to AD risk, informing prevention and mechanistic hypotheses.
Toyli A, Zhao C, Su KJ et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗
Metabolism, Mitochondria & Cellular Bioenergetics
Complete biosynthesis of the anticancer cephalotaxinone and homoerythratine.
This study investigated the complete biosynthetic pathways for cephalotaxinone and homoerythratine, natural products related to homoharringtonine (HHT), using comprehensive multi-omics analysis and chemically synthesized standards to identify missing enzymes. The key finding was the identification of the previously unknown enzymes required to reconstruct full biosynthesis of these alkaloids. This provides a route toward scalable production of HHT-related compounds from biosynthetic engineering rather than limited natural sources.
Tian R, Lin F, Guo N et al. · Cell · (2026) · View on PubMed ↗
RND3 Enhances Cardiac Glucose Metabolism Through Inhibiting ACAT1-Dependent PDHA1 Acetylation and Protects Against Ischemia-Reperfusion Injury.
This study investigated how the small GTPase RND3 regulates cardiac glucose metabolism and mitochondrial PDHA1 acetylation in a murine model of myocardial ischemia-reperfusion (I/R) injury, using cardiomyocyte-specific Rnd3 knockout and Rnd3 overexpression. RND3 enhanced glucose metabolism by inhibiting ACAT1-dependent PDHA1 acetylation and reduced injury in the I/R setting. These results identify an RND3–ACAT1–PDHA1 axis as a potential therapeutic target to protect cardiac energy metabolism during ischemic stress.
Xiong Z, Li Y, Zhang Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗
Discovery of a snail hibernation-inducer offering hibernation-like cardioprotection through metabolic rewiring and autophagy in mice.
This work discovered and tested a circulating dormancy-inducing factor from hibernating snails in mice, focusing on metabolic rewiring and autophagy during ischemia/ischemia-reperfusion (IR) injury. The chemically synthesized factor, SNAP, activates PHLPP1 to dephosphorylate mitochondrial p-AKT and cytoplasmic p-S6K1, inducing a reversible dormancy-like state and promoting autophagy and proteostasis during IR. The results support SNAP/PHLPP1 as a first-in-class strategy for cardioprotection via dormancy and autophagy rather than continuous pathway inhibition.
Piao J, Zhang Y, Zhao YY et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
A first-in-class pulsatile FXR agonist for bile-acid-related liver diseases.
This paper reports the design and preclinical evaluation of linafexor, a first-in-class pulsatile farnesoid X receptor (FXR) agonist for bile-acid-related liver diseases, engineered for rapid systemic clearance to drive cyclic rather than continuous FXR activation. In multiple metabolic dysfunction-associated steatohepatitis and liver fibrosis models, pulsatile linafexor produced robust efficacy while aiming to avoid toxicity associated with sustained nuclear receptor activation. These results support pharmacokinetic “pulsing” as a generalizable strategy to improve safety and effectiveness of FXR-targeted therapies.
Zang Y, Shi J, Zhao G et al. · Nature · (2026) · View on PubMed ↗
Diverse binding poses of agonistic neurotoxins on human Nav1.6.
This structural study used cryo-electron microscopy to determine distinct binding poses of three agonistic peptide toxins on the human Nav1.6–β1 channel complex. The toxins occupy different locations relative to the voltage-sensing domain and pore extracellular loops, revealing how multiple binding geometries can produce agonistic effects on Nav1.6. These structures provide mechanistic templates for designing therapeutics that target Nav1.6 using toxin-inspired binding modes.
Fan X, Huang J, Yang L et al. · Nature · (2026) · View on PubMed ↗
Mitochondria directly interact with the nuclear pore complex.
This study investigated whether mitochondria physically interact with the nuclear pore complex (NPC) by combining unbiased proteomic approaches (GST pulldown and BioID) with cell biology assays. It identified VDAC1 as a top mitochondrial candidate interacting with a filamentous nuclear pore component and demonstrated direct mitochondria–nuclear pore interactions. The work suggests a new organelle crosstalk pathway that could regulate nuclear transport and pro-survival signaling through mitochondrial–NPC coupling.
Menendez-Montes I, Marin-Vicente C, Mukherjee S et al. · Nature · (2026) · 1 citations · View on PubMed ↗
Cryo-EM structures of Drosophila OR67d-Orco complexes reveal insect pheromone sensing mechanism.
The study investigated mitochondrial iron supply mechanisms by focusing on mitochondria–ER contact sites (MERCs) and the roles of haem metabolism and iron-handling proteins in cells. It found that haem oxygenase 2 (HMOX2), an ER-resident enzyme, localizes to MERCs and supports haem-derived iron delivery to mitochondria, while the mitochondrial ubiquitin ligase MITOL (MARCH5/MARCHF5) orchestrates this process to maintain mitochondrial iron homeostasis and supercomplex integrity. This reveals a MERC-based pathway for iron transfer that could be targeted to modulate mitochondrial metabolism and related diseases.
Wang J, Yang C, Chang S et al. · Cell research · (2026) · View on PubMed ↗
Mitochondria-ER contacts function as an iron supply hub.
The study used cryo-EM to determine structures of Drosophila pheromone receptor complexes OR67d–Orco in multiple states, including apo closed, pheromone-bound open, and the synthetic agonist VUAA1-bound open conformations. It found that OR67d and Orco assemble into a hetero-tetrameric channel with a 1:3 stoichiometry and that the cVA ligand (or analog) binds in a deep, bent pocket within OR67d. These structural insights explain how insect pheromone binding is converted into receptor-channel activation, advancing the molecular basis of pheromone sensing.
Oshio H, Shiiba I, Ito N et al. · Nature cell biology · (2026) · View on PubMed ↗ · Free PDF ↗
eIF3 Orchestrates a Biphasic Stress Response Linking Translational Control to Mitochondrial Integrity in Skeletal Muscle.
This study investigated how the eukaryotic translation initiation factor 3 (eIF3) complex coordinates a biphasic stress response that links translational control to mitochondrial integrity in skeletal muscle. It identified eIF3-dependent regulation of translation programs and mitochondrial homeostasis across distinct stress phases, demonstrating that specific eIF3 dynamics are required for proper mitochondrial preservation under stress. The scientific significance is that it connects a major translation regulator (eIF3) to mitochondrial resilience mechanisms relevant to muscle adaptation and disease.
Lin Y, Xia J, Li M et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗
Infectious Disease & Host–Pathogen Interactions
Clinical Features, Treatment Outcomes, and Cytokine Levels in Pediatric Tularemia Patients in Türkiye.
This multicenter prospective study evaluated clinical features, treatment outcomes, and cytokine dynamics in pediatric tularemia in Türkiye using serum immune profiling. It enrolled 40 laboratory-confirmed pediatric tularemia patients and 9 matched healthy controls and measured treatment-associated changes in cytokines including IL-6 and IL-2. The results help define pediatric disease phenotype and immune signatures that may inform prognosis and optimize treatment strategies for this rare zoonosis.
Cakici O, Aykac K, Seyrek BE et al. · The American journal of tropical medicine and hygiene · (2026) · View on PubMed ↗
Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.
This study examined how major fungal pathogens Candida albicans and Candida auris induce macrophage dysfunction and death via host glucose starvation, identifying the role of the executioner protein NINJ1. It found that glucose-starved macrophages activate NINJ1 to rupture membranes independently of known cell-death programs, and that alanine supplementation rescues macrophages by inhibiting NINJ1 oligomerization. Scientifically, it links pathogen-driven metabolic competition to a specific NINJ1-dependent mechanism of macrophage lysis and fungal escape.
Weerasinghe H, Tulyaprawat O, Stölting H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Promotion of hepatitis B virus infection by extracellular apolipoprotein E.
This study investigated how extracellular apolipoprotein E (apoE) promotes hepatitis B virus (HBV) infection, building on prior findings that human apoE is incorporated into infectious HBV virions. The key finding is that apoE enhances HBV infection by mediating viral attachment to host cell receptors, including LDL receptor (LDLR) family members and heparan sulfate proteoglycans (HSPGs), and that HBV-associated apoE and hepatocyte apoE expression are required for efficient infection. These results identify apoE–receptor interactions as potential therapeutic targets to limit HBV entry and chronic infection.
Elgendy E, Tripathi SK, Luo G · Journal of virology · (2026) · View on PubMed ↗ · Free PDF ↗
Adaptive mutations at lysine residues of PRRSV-2 nsp12 enable evasion of host proteasomal degradation to promote subgenomic RNA synthesis.
This mechanistic study examined how adaptive mutations at lysine residues in PRRSV-2 nonstructural protein 12 (nsp12) enable evasion of host proteasomal degradation to promote subgenomic RNA synthesis. It found that nsp12 is targeted for ubiquitin-proteasome degradation via K48- and K63-linked polyubiquitination at lysines 89, 91, 127, and 130, and that RNF114 functions as the E3 ubiquitin ligase involved. The work clarifies a viral immune-evasion strategy that could inform antiviral approaches targeting ubiquitination/proteasome control of PRRSV replication.
Chen Y, Chen Z, Huang L et al. · Journal of virology · (2026) · View on PubMed ↗ · Free PDF ↗
Microbiome, SCFAs & Gut–Immune Axis
Dietary fat alters goblet cell function and microbial bile acid metabolism to promote intestinal lipid absorption in mice.
This study used mouse models of diet-induced and genetic obesity to determine how dietary fat reshapes the colonic mucus niche and host–microbiota bile-acid metabolism, using multi-omics and analyses of goblet-cell function. Excess dietary lipids impaired goblet-cell glutamine metabolism and redox homeostasis, thinning the mucus layer, depleting Akkermansia muciniphila, and expanding the bile-acid-transforming bacterium Clostridium scindens, with enterohepatic bile-acid changes activating an FXR–PLIN2 signaling axis. These findings identify the mucus niche as an early, diet-sensitive driver of metabolic dysfunction and suggest bile-acid/FXR–PLIN2 and mucus–microbe interactions as therapeutic targets to improve intestinal lipid absorption and obesity-related disease.
Liang X, Zhang Y, Xie W et al. · Nature microbiology · (2026) · View on PubMed ↗
Microbiota-driven gut-brain signaling underlies antidepressant effects of a GLP-1 analog.
The study tested whether the GLP-1 analog liraglutide produces antidepressant effects via a gut-brain pathway independent of GLP-1R, using pharmacologic and genetic mouse models plus microbiota manipulations. Liraglutide retained antidepressant efficacy in Glp1r-/- mice and in mice treated with the GLP-1R antagonist Exn9, but gut microbiota depletion abolished the effect, and multi-omics linked liraglutide to increased Lactobacillus delbrueckii abundance and restoration of downstream endocannabinoid-related changes. This supports a microbiota-mediated mechanism for liraglutide’s antidepressant action that could inform non-GLP-1R therapeutic strategies for depression.
Bian L, Cai Y, Zhang Y et al. · Cell host & microbe · (2026) · View on PubMed ↗ · Free PDF ↗
Gut microbiota-derived short-chain fatty acids (SCFAs): immunomodulatory effects and therapeutic potential in infections.
This comprehensive literature analysis evaluated how gut microbiota-derived short-chain fatty acids (SCFAs) modulate immunity and barrier function and how they interact with 11 key pathogens (including Staphylococcus aureus, Clostridioides difficile, Salmonella spp., Campylobacter jejuni, Klebsiella pneumoniae, Vibrio cholerae, Candida albicans, SARS-CoV-2, influenza virus, respiratory syncytial virus, and rotavirus). Across the reviewed evidence, SCFAs showed immunomodulatory and anti-pathogen effects that suggest therapeutic potential in infections. The findings support further translational studies of SCFA-based or microbiome-targeted interventions to prevent or treat infectious diseases.
Yu J, Li W, Xu Y et al. · Clinical microbiology reviews · (2026) · View on PubMed ↗ · Free PDF ↗
Inflammation, Autoimmunity & Immune-Mediated Disease
Charting human cellular senescence in aging and disease.
This article reviewed and synthesized approaches for mapping cellular senescence across human tissues in aging and disease using single-cell and spatial multi-omics combined with AI-driven analyses. The key finding is that these integrated methods can chart senescent cell heterogeneity (“senotypes”), revealing tissue-specific senescence programs and senescence–microenvironment interactions. This framework supports biomarker discovery and the development of targeted senotherapeutic strategies.
Suryadevara V, Farzad N, Yang M et al. · Cell · (2026) · View on PubMed ↗
Persistent and transient senescent cells contribute to brain-barrier development.
The study examined developmentally programmed p21+ senescent cells in mice and how their senescence states differ across the choroid plexus (blood-CSF barrier) versus brain vasculature and brain-resident macrophages (blood-brain barrier). Choroid plexus epithelial cells adopted a lifelong, non-inflammatory p21+ senescent state supporting CSF production and blood-CSF barrier integrity, whereas vascular endothelial cells and macrophages showed transient, pro-inflammatory senescence profiles during vascularization with reciprocal signaling. These findings suggest that temporally and spatially distinct senescent-cell programs are actively required for normal brain-barrier development and may represent targets for barrier-related disorders.
Watson LA, Adelsheim Z, Carter MJ et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗
Potential regulation of kynurenine pathway metabolism by the galantamine-memantine combination in rheumatologic diseases: A hypothesis-driven review.
This hypothesis-driven review evaluated whether the galantamine–memantine combination, with or without N-acetylcysteine (NAC), could regulate kynurenine pathway (KP) metabolism relevant to rheumatologic inflammatory diseases. The authors propose that modulating nicotinic receptors (galantamine) and NMDA signaling (memantine), potentially alongside antioxidant/anti-inflammatory effects from NAC, may shift KP metabolism in ways that could influence systemic inflammation. If validated experimentally and clinically, this combination could provide a novel KP-targeted therapeutic approach for rheumatologic disorders.
Mathew N, George S, Rejimon P et al. · The Journal of pharmacology and experimental therapeutics · (2026) · View on PubMed ↗
Interleukin-10 Autoantibodies and HLA-DRB1*01:03 in Inflammatory Bowel Disease.
This study investigated whether neutralizing interleukin-10 (IL-10) autoantibodies and the genetic risk allele HLA-DRB1*01:03 are associated with inflammatory bowel disease (IBD) in children and other cohorts. Using a cellular IL-10 reporter assay, confirmatory competitive ELISA, and an in vitro cytokine-release bioassay in a subgroup, the authors assessed the presence and functional impact of neutralizing IL-10 autoantibodies in IBD patients versus controls. The work is clinically important because identifying IL-10 autoantibody–mediated disease could enable more precise diagnosis and potentially targeted immunologic treatment for a subset of IBD patients.
Gharahdaghi N, Yeh PJ, Ceron-Gutierrez L et al. · The New England journal of medicine · (2026) · 1 citations · View on PubMed ↗
The Impact of Hidradenitis Suppurativa on Sexual Function: A Multicentered Cross-Sectional Study.
This multicentered cross-sectional study assessed sexual dysfunction in patients with hidradenitis suppurativa (HS) and examined associations with disease and patient characteristics using structured online questionnaires and validated HS instruments. The key finding was the measured rate of sexual dysfunction among HS patients and its relationship to HS severity/impact captured by tools such as the Hidradenitis Suppurativa Self-Assessment Tool (HSSA) and HS-specific quality-of-life measures. Clinically, it highlights sexual health as an important, quantifiable comorbidity in HS that should be addressed in patient care.
Özkoca D, Eker H, Ak DY et al. · International journal of dermatology · (2026) · View on PubMed ↗ · Free PDF ↗
Effect of depemokimab on asthma control and clinical outcomes: a systematic review and meta-analysis of randomized controlled trials.
This systematic review and meta-analysis synthesized randomized controlled trials comparing depemokimab (a long-acting anti–interleukin-5 monoclonal antibody) versus placebo in eosinophilic asthma. It assessed effects on asthma control (ACQ-5), exacerbation rates, quality of life (SGRQ), and adverse events. The significance is that it consolidates evidence on whether depemokimab improves broader clinical outcomes beyond exacerbation reduction in eosinophilic asthma.
Nakahara S, Hallack Moura MJ, Cengiz SK et al. · Expert review of respiratory medicine · (2026) · View on PubMed ↗
Reproductive Biology, Development & Assisted Reproduction
Two distinct causes contribute to the low efficiency of human pre-implantation development.
This study investigated the causes of low efficiency in human pre-implantation development by imaging ~150 live human and monkey fertilized eggs up to 5 days and analyzing mitotic errors. It found that the second mitotic division was the most error-prone, with stochastic centriole overduplication leading to multipolar spindle formation, chromosome missegregation, and micronucleus formation in human embryos. The finding that centriole overduplication can be suppressed by transient PLK4 inhibitor centrinone highlights a mechanistic target to improve embryo developmental competence in assisted reproduction.
Li Z, Leng L, Zhai J et al. · Cell · (2026) · View on PubMed ↗
DNA repair drives cisplatin-induced neuronal death.
This study developed a continuous in vitro modeling system of primate embryogenesis by generating primate organogenetic embryoids from cynomolgus totipotent blastomere-like stem cells (cTBLCs). It found that cTBLCs spontaneously form blastoids that progress through gastrulation to early organogenesis, producing neural-tube-like structures and cardiac-like beating. The work is significant for providing a scalable primate model spanning totipotency to early organogenesis for studying early developmental biology.
Nathan WJ, Chen C, Sakr R et al. · Cell · (2026) · View on PubMed ↗
Musculoskeletal, Bone & Muscle Aging
The post-reproductive ovary shifts from a reproductive to an immune-like organ.
This study used paired histology and bulk transcriptomics to characterize ovarian aging in mice, comparing reproductively young (2 months), reproductively old (18 months), and post-reproductive (24 months) ovaries. It found a shift from reproductive functionality toward an immune-dominant ovarian signature with age, alongside stromal remodeling and increased collagen deposition after follicle exhaustion. These findings suggest that the post-reproductive ovary becomes an immune-like organ, informing how reproductive aging may drive systemic inflammatory changes.
Converse A, Dipali SS, Schowe IP et al. · Molecular human reproduction · (2026) · View on PubMed ↗
A decline in skeletal muscle NOX4 abrogates exercise-induced adaptive homeostasis and exacerbates biological aging.
The study examined how age-related decline of the NADPH oxidase isoform NOX4 in skeletal muscle affects NFE2L2-driven adaptive homeostasis and aging phenotypes in both aged mice and humans. It found that NOX4 levels decline with age, leading to impaired NFE2L2 adaptive responses, increased protein oxidative damage, reduced muscle function, and that skeletal muscle–specific NOX4 deletion worsened aging outcomes including sarcopenia and frailty. Scientifically, it identifies NOX4 as a key regulator of exercise-linked redox adaptation and suggests that preserving NOX4–NFE2L2 signaling could mitigate biological aging and muscle decline.
Xirouchaki CE, García-Domínguez E, Coughlan E et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
3,4-Dimethoxychalcone Protects Against Steroid Induced Femoral Head Necrosis by Suppressing Ferroptosis via Activation of STAT3-Nrf2 Signaling Pathway.
This preclinical study tested whether 3,4-dimethoxychalcone (3,4DC) protects against dexamethasone-induced femoral head necrosis by suppressing ferroptosis via activation of the STAT3–Nrf2 signaling pathway in a rat model. The key finding was that 3,4DC reduced Dex-induced ferroptosis and ameliorated femoral head necrosis, with mechanistic support for STAT3–Nrf2 pathway involvement. Scientifically and therapeutically, it positions 3,4DC as a candidate intervention for glucocorticoid-induced osteonecrosis by targeting ferroptotic cell death.
Han LJ, Miao JS, Wu SH et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗
Therapeutic Delivery Platforms (Vectors, Nanomedicine, Gene/Cell Therapy)
Skeletal-muscle-targeted non-viral delivery of full-length DMD mRNA for Duchenne muscular dystrophy.
This study investigated systemic, skeletal-muscle-targeted non-viral delivery of full-length DMD mRNA in a murine model of Duchenne muscular dystrophy using allogenically engineered targeting extracellular vesicles (DMD t-EVs). The key finding was that DMD t-EVs enabled delivery of full-length DMD mRNA to restore dystrophin expression in skeletal muscle without the packaging limitations typical of viral vectors. This supports a potentially safer, non-integrating mRNA strategy for DMD that could overcome viral vector toxicity/immunogenicity and enable full-length dystrophin restoration.
Tian Y, Liu Y, Tong Y et al. · Nature biomedical engineering · (2026) · View on PubMed ↗
Exa-cel in Children with Transfusion-Dependent β-Thalassemia or Sickle Cell Disease.
This phase 3 program evaluated exagamglogene autotemcel (exa-cel) in children aged 5 to 11 years with transfusion-dependent β-thalassemia or sickle cell disease, using ex vivo CRISPR-Cas9 editing of an erythroid-specific enhancer region of BCL11 in autologous CD34+ cells to induce fetal hemoglobin. The key finding was that exa-cel eliminated vaso-occlusive crises and reduced the need for red-cell transfusions in this pediatric age group, consistent with prior older cohorts. Clinically, it extends a gene-editing cell therapy option to younger children with hemoglobinopathies who previously had limited curative access.
Frangoul H, de la Fuente J, Chopra Y et al. · The New England journal of medicine · (2026) · View on PubMed ↗
Intrinsically Mitochondria-Targeting Nanozyme via Coordination-Assembly of Natural Quercetin for Cascade Antioxidant Therapy of Cerebral Ischemia-Reperfusion Injury.
This work engineered an intrinsically mitochondria-targeting nanozyme by coordinating natural quercetin to deliver cascade antioxidant therapy for cerebral ischemia-reperfusion injury, targeting the mitochondrial outer membrane. The authors leveraged quercetin’s intrinsic mitochondrial binding to create an ultrasmall mitochondria-targeting cascade nanozyme designed to interrupt oxidative stress–driven mtDNA release and downstream inflammation. Scientifically, it advances a quercetin-based mitochondrial targeting strategy that could improve antioxidant efficacy in neurovascular ischemia-reperfusion injury.
Zheng W, Wang Z, Zhou X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Dual-target gene therapy in Parkinson’s disease: a multicenter phase 1 trial.
This multicenter, open-label phase 1 trial evaluated the safety and tolerability of BBM-P002, an AAVT42 vector delivering dual gene therapy for Parkinson’s disease targeting tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC). The study reports 12-month primary outcomes for dose-escalation administration, aiming to enable autonomous striatal dopamine synthesis without reliance on exogenous levodopa. If safe, this dual TH/AADC AAV strategy could overcome limitations of AADC-only monotherapy and address AAV packaging constraints in multigene delivery.
Niu M, Guo J, Yang Y et al. · Nature medicine · (2026) · View on PubMed ↗
In vivo base editing alleviates hepatic iron accumulation and fibrosis in models of HFE-related hereditary hemochromatosis.
This preclinical study tested in vivo base editing for HFE-related hereditary hemochromatosis by correcting the HFE C282Y loss-of-function mutation in a murine model under iron challenge, using lipid nanoparticles (LNPs) delivering base editor mRNA and sgRNA. It found that base editing alleviated hepatic iron accumulation and reduced liver fibrosis, with parallel editing performed in patient-derived iPSCs and hepatocyte-like cells using the same approach. Clinically, it supports mutation-specific, liver-targeted RNA/DNA editing as a potential disease-modifying therapy for C282Y hemochromatosis.
Hamann V, Hook S, Sujariyakul P et al. · Journal of hepatology · (2026) · View on PubMed ↗ · Free PDF ↗
Subretinal Gene Therapy for X-Linked Retinoschisis.
This clinical study evaluated subretinal gene therapy for X-linked retinoschisis by injecting a single AAV8 vector carrying human RS1 cDNA (scAAV8-hRS1) into one eye of patients aged 5–18 years. The primary endpoint was safety through 52 weeks, with secondary outcomes including changes in best-corrected visual acuity and retinal structure/function measured by swept-source OCT and functional testing of photoreceptors and bipolar cells. The results are significant because they test whether RS1 gene replacement via AAV8 can be safely delivered and improve vision in pediatric patients with a monogenic retinal disease.
Liang L, She K, Ren C et al. · The New England journal of medicine · (2026) · View on PubMed ↗
CRISPR-Based Gene Therapy for Brain Disease.
This review article surveys CRISPR-Cas9–based gene therapy approaches for brain diseases caused by pathogenic gene mutations, describing editing across diverse cell types and model systems. It reports that CRISPR-Cas9 enables precise, programmable gene editing and is increasingly being developed to move beyond symptom-only treatments toward mechanism-based interventions. The work is significant for guiding translational research on how to design and deploy CRISPR therapies for neurological disorders.
Khajouei F, Ghaemi A, Abnous K et al. · Molecular neurobiology · (2026) · View on PubMed ↗
Generated automatically on June 12, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.