PubMed Trending Research Digest — July 04, 2026

Automated digest · 99 articles · 15 research areas · July 04, 2026

Overview

Across this week’s set of studies, a dominant theme is how physical and spatial context—mechanical forces, tissue architecture, and microenvironmental organization—feeds into cell fate decisions and disease progression. Multiple papers connect mechanotransduction to regeneration or pathology (PIEZO1 and hepatocyte zonation in liver regrowth; ECM stiffening driving endothelial senescence; lysosomal repair under mechanical/osmotic stress; ovarian matrix stiffening via IL-11), while others use spatially patterned organoid systems or spatial multi-omics to explain how geometry and niche boundaries govern development and tumor behavior.

A second major thread is immune regulation as an organizer of outcomes, spanning immune–stromal circuits, immune exclusion, and immune evasion. Studies describe how ILC2s control pancreatic fibroblast progenitors, how tumor-intrinsic signaling axes (eATP–P2RY2–COX–PGE2; YAP/TAZ→Tgfb2; EV-driven macrophage polarization; mitochondrial STING–metabolic reprogramming) reshape immune infiltration and therapy response, and how viral proteins (HSV-1 UL16) suppress innate interferon signaling. Together, these findings emphasize that “immunity” is not only about immune cells in isolation, but about the biochemical and mechanical programs that tune their access, activation state, and persistence.

Finally, the digest highlights accelerating translational momentum in diagnostics, risk prediction, and targeted therapy. Several works improve detection or stratification—OCT rules for glaucoma in myopia, methylated SEPT9 for HCC surveillance, amyloid PET governance frameworks, frailty/biological aging measures, and PRS/prognostic models in IPF and AML. On the therapeutic side, the week includes mechanistic and clinical advances in oncology (CDK2 inhibition for CDK4/6-resistant breast cancer, CAR-T schedule optimization and engineering, radionuclide vs targeted therapy comparisons) and in supportive/adjunct strategies (cachexia neurobiology, lifestyle/GLP-1 mechanistic links to appetite, and standardized clinical pathways).

---

Mechanobiology & Tissue Mechanics

Modulating IL-11-dependent matrix stiffness to delay ovarian aging.

This study examined how IL-11-dependent changes in ovarian extracellular matrix mechanics affect ovarian aging using atomic force microscopy (AFM) in human ovarian tissues and mechanistic profiling of human ovarian fibroblasts. It found that ovarian matrix stiffness increases with aging and in conditions including chemotherapy-induced premature ovarian insufficiency (POI), polycystic ovary syndrome (PCOS), and ovarian endometriosis, and it identified IL-11 as a key elevated factor in aging ovaries. By linking IL-11 to matrix stiffening, the work suggests a potential target to delay or mitigate ovarian functional decline.

Wu M, Zhu Q, Xiong J et al. · Nature aging · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Regional organization of nutrient absorption across the small intestine.

This Review summarizes how nutrient absorption in the small intestine is organized regionally along the longitudinal and apical–basal axes at molecular, cellular, and functional levels. It emphasizes epigenetic and transcriptional features of intestinal zonation and discusses mechanisms that establish and maintain regional gene expression programs during development. The significance is a unified framework for understanding how spatial compartmentalization supports both absorption and barrier protection.

Zwick RK, Sharpley M, Rispal J et al. · Nature reviews. Gastroenterology & hepatology · (2026) · View on PubMed ↗

VPS13C/PARK23 initiates lipid transfer and membrane remodeling for efficient lysosomal repair.

This study examined how the bridge-like lipid transport protein VPS13C/PARK23 functions in lysosomal repair in cells under mechanical or osmotic lysosome stress. VPS13C binds lysosomes in anticipation of membrane lesions, and its C-terminal ATG2C domain senses damage-induced lipid packing defects to drive ER-lysosome contact–dependent lipid transfer and membrane remodeling. The work identifies VPS13C/PARK23 as a key early lysosomal repair node, with implications for neurological disorders and aging linked to lysosome integrity failure.

Adeosun OA, Schröer C, Südhoff E et al. · Nature communications · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Matrix Stiffness Induces Endothelial Network Senescence.

This study examined how extracellular matrix (ECM) stiffening drives endothelial cell (EC) senescence using a 3D human in vitro model designed to isolate mechanical stress from inflammatory/biochemical cues. Matrix stiffening induced an EC senescence phenotype characterized by increased p16/p21 and a senescence-associated secretory phenotype (SASP) without inflammatory signals. The results support ECM mechanical cues as a direct driver of vascular aging and highlight potential targets for restorative interventions aimed at preventing endothelial dysfunction.

Song J, Rindone AN, Guan Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

---

Liver Regeneration & Hepatocyte Proliferation

The mechanics of liver regeneration.

The study investigated how mechanosensitive ion channels regulate hepatocyte proliferation during liver regeneration after injury in vivo. It found that a specific mechanosensitive ion channel controls the regenerative proliferative response of liver cells. These findings identify a mechanotransduction node that could be targeted to improve or modulate regenerative outcomes after liver damage.

Maeso-Diaz R, Diehl AM · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Zonated mechanosensing by PIEZO1 controls liver regeneration.

The study examined how tissue mechanics coordinate zonated hepatocyte proliferation during mouse liver regeneration. It found that mechanosensing by PIEZO1 in zone 2 DPP4+ hepatocytes integrates biomechanical cues to drive regrowth via IGFBP2, and that genetic disruption of PIEZO1 restrains hepatocyte proliferation. These results identify PIEZO1-mediated mechanotransduction as a zonation-specific control mechanism for effective liver regeneration.

Zhang Y, Sun Y, Xu G et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗

---

Immune–Stromal & Tumor Microenvironment (TME) Crosstalk

Duchenne Muscular Dystrophy and Delandistrogene Moxeparvovec Gene Therapy in Children: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated efficacy of delandistrogene moxeparvovec gene therapy in ambulatory pediatric patients with Duchenne muscular dystrophy (DMD) caused by DMD pathogenic variants. The pooled evidence assessed outcomes intended to reflect restoration of dystrophin/microdystrophin expression and functional benefit in children receiving the therapy. By synthesizing trial data, the study helps quantify the clinical effectiveness of this microdystrophin gene therapy for ambulatory DMD patients and informs expectations for treatment impact.

Antonello BB, Cargnelutti Fontoura F, Braga Albuquerque AL et al. · Neurology. Genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Dual-modular-nanobody CAR-T cell technical platform against the solid tumor microenvironment.

This preclinical study developed a dual-modular nanobody-based CAR-T platform targeting fibroblast activation protein (FAP) on cancer-associated fibroblasts and locally releasing an anti-CTLA-4 nanobody within the solid tumor microenvironment. In vitro assays assessed antigen-specific cytotoxicity, cytokine release, and exhaustion, and in vivo xenograft experiments evaluated antitumor efficacy. The approach aims to improve solid-tumor CAR-T performance by combining TME targeting (FAP) with localized CTLA-4 blockade to enhance activity while reducing systemic toxicity.

Li Y, Wang X, Zhang S et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Matching-Adjusted Indirect Comparison of Risankizumab Versus Icotrokinra in Adult Patients with Moderate-to-Severe Plaque Psoriasis.

This matching-adjusted indirect comparison (MAIC) compared risankizumab (an IL-23 inhibitor) versus icotrokinra (an oral IL-23 receptor blocker) in adult patients with moderate-to-severe plaque psoriasis using individual patient data from risankizumab phase 3 trials and published icotrokinra phase 3 summary data. The analysis estimated placebo-adjusted response differences through week 52 for clinically relevant endpoints (including ≥75% skin clearance thresholds). The results provide comparative effectiveness estimates in the absence of head-to-head trials to inform treatment decisions between IL-23 pathway agents.

Crowley J, Song EJ, Stein-Gold L et al. · Dermatology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Single-Cell dissection of fibrodysplasia ossificans progressiva identifies SPP1 as a mediator of macrophage-fibroadipogenic progenitors crosstalk.

This study used a tamoxifen-inducible Acvr1R206H mouse model of fibrodysplasia ossificans progressiva (FOP) with a muscle injury protocol and single-cell RNA sequencing plus in vitro assays to map early immune–progenitor interactions during lesion formation. It found macrophage and fibro-adipogenic progenitor (FAP) expansion and identified SPP1 as a mediator of macrophage–FAP crosstalk. These results implicate SPP1-driven immune–stromal signaling as a mechanistic lever for preventing or modulating inflammatory flare-associated heterotopic ossification in FOP.

Gamberale R, Bergamaschi M, Tascini AS et al. · Cellular and molecular life sciences : CMLS · (2026) · View on PubMed ↗ · Free PDF ↗

A guide to CAR T cell therapies: development, current status and future prospects.

This review summarizes the development and clinical status of chimeric antigen receptor (CAR) T cell therapies in patients with B cell malignancies and discusses emerging next-generation approaches. It reports that CAR T therapies approved since 2017 have produced durable remissions in B cell leukemias, lymphomas, and multiple myeloma, while future directions include gene editing, allogeneic manufacturing, and in vivo delivery to expand use to autoimmune disease and solid tumors. The synthesis highlights how engineering and manufacturing innovations are improving scalability and safety, guiding translation toward broader indications.

Rafei H, Upadhyay R, Sharma P · Nature reviews. Immunology · (2026) · View on PubMed ↗

Single cell spatial transcriptomics track the evolutionary hierarchy and microenvironment remodeling during breast carcinoma invasion.

This study used single-cell RNA sequencing, spatial transcriptomics, and genomics across 28 patients with synchronous ductal carcinoma in situ (DCIS) and invasive breast carcinoma (IBC) to map the evolutionary hierarchy and tumor microenvironment remodeling during invasion. IBC progression was driven mainly by clonal expansion of pre-existing DCIS subclones, with transcriptional reprogramming and tumor microenvironment (TME) remodeling (including epithelial-mesenchymal transition and metabolic reprogramming) rather than acquisition of additional driver alterations. These results support a model of invasion as a spatially organized evolutionary process that could inform stage-specific therapeutic targeting.

Wang D, Dai Q, Guo J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.

This study analyzed human psoriatic lesions and used single-cell RNA sequencing and immunofluorescence to determine how macrophage insulin-induced gene 1 (INSIG1) influences psoriasiform dermatitis, followed by in vivo myeloid-specific Insig1 deficiency experiments. INSIG1 expression was specifically reduced in macrophages in psoriatic skin, and myeloid-specific Insig1 deficiency exacerbated disease through a SREBP2–STAT1 inflammatory axis. The findings connect cholesterol-regulatory control in macrophages to psoriasis pathogenesis, suggesting INSIG1/SREBP2/STAT1 pathway modulation as a potential therapeutic strategy.

Li X, Zang Y, Li X et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

[177Lu]Lu-edotreotide versus everolimus for gastroenteropancreatic neuroendocrine tumours (COMPETE): a phase 3, multicentre, randomised, open-label, superiority trial.

The COMPETE phase 3, multicentre, randomized, open-label superiority trial compared [177Lu]Lu-edotreotide (a peptide receptor radionuclide therapy) versus everolimus (a targeted molecular therapy) in adults with metastatic, somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors (GEP NETs), including treatment-naive or previously treated grade 1–2 disease. The study evaluated comparative efficacy and harms to determine preferred sequencing between radionuclide therapy and everolimus. This directly informs treatment strategy for advanced GEP NETs by testing which targeted approach yields better outcomes in this defined patient population.

Walter T, Jann H, Ansquer C et al. · Lancet (London, England) · (2026) · 1 citations · View on PubMed ↗

Autologous and allogeneic haematopoietic cell transplantation in adult patients with Hodgkin lymphoma: recommendations from the EBMT Practice Harmonisation and Guidelines Committee and Lymphoma Working Party.

This EBMT Practice Harmonisation and Guidelines Committee consensus guideline, developed by expert panels for Hodgkin lymphoma, addressed the use of autologous and allogeneic hematopoietic cell transplantation (HCT) in adults with relapsed or refractory Hodgkin lymphoma. The guideline provides structured recommendations across major clinical decision points, including salvage therapy considerations (e.g., incorporating brentuximab vedotin) and transplant selection. Scientifically and clinically, it harmonizes transplant practice to improve decision-making and outcomes for HL patients who need HCT.

Bazarbachi A, Advani R, Ahmed S et al. · The Lancet. Haematology · (2026) · View on PubMed ↗

Spatially defined microenvironmental niches are associated with clinical outcome and tumor ecosystem diversity in head and neck cancer.

This study profiled 44 primary head and neck squamous cell carcinoma (HNSCC) tumors using single-cell spatial transcriptomics and spatial proteomics to map tumor, immune, and stromal organization into spatially defined microenvironmental niches. Integrated computational analyses identified spatial niches and ecosystem states that were associated with clinical outcome and tumor ecosystem diversity, beyond HPV status alone. These results suggest that spatial microenvironment architecture can serve as a prognostic and mechanistic framework for HNSCC heterogeneity.

An J, Hu E, Shen Q et al. · Med (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

Factors Associated With Disability Improvement and Worsening Independent of Attacks in Patients With AQP4-IgG+ NMOSD and MOGAD: A Multicenter Cohort Study.

This multicenter retrospective cohort study assessed disability trajectories in patients with AQP4-IgG+ neuromyelitis optica spectrum disorder (NMOSD) and MOGAD, focusing on confirmed disability improvement (CDI) and confirmed disability worsening (CDW) independent of attacks. CDI frequency and CDW independent of attacks were quantified, and clinical factors associated with these non-attack-driven disability changes were identified. The results refine prognostication for AQP4-IgG+ NMOSD and MOGAD by separating attack-related damage from other disease processes that can still alter disability.

Engels D, Schindler P, Havla J et al. · Neurology · (2026) · View on PubMed ↗ · Free PDF ↗

ILC2s regulate a fibroblast progenitor niche in the pancreas.

The study examined how group 2 innate lymphoid cells (ILC2s) regulate pancreatic fibroblast development and spatial niche organization during homeostasis and inflammation. It found that ILC2s colocalize with and specifically control expansion of Pi16+Dpp4+Ly6c+ progenitor-like fibroblasts while restraining differentiation into Col15a1+ intraparenchymal fibroblasts during injury. This defines an immune–stromal circuit that restores fibroblast numbers after pancreatic damage and may inform anti-fibrotic or regenerative strategies.

Yip T, Stockis J, Simpson C et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

Patterning human kidney organoids with synthetic Wnt-secreting organizers.

The study used spatial transcriptomics of human kidney development and engineered WNT-secreting cellular organizers to impose spatial patterning in human kidney organoids. It found that nascent nephrons establish collecting-duct adjacency and polarity across a WNT11–WNT9B signaling boundary, and that introducing synthetic WNT11/WNT9B organizers into organoids restored organizing geometry. This demonstrates a rational, organizer-based approach to improve reproducible spatial organization in stem-cell-derived kidney organoids.

Fausto CC, Glykofrydis F, Kumar N et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

Extracellular matrix reprogramming by the YAP/TAZ- TGF-ß2 axis drives immune exclusion in cholangiocarcinoma models.

The study investigated how the YAP/TAZ–TGF-β2 axis remodels extracellular matrix to drive immune exclusion in translational cholangiocarcinoma models. It found that sustained systemic YAP/TAZ depletion caused severe side effects, whereas pulsed inhibition suppressed tumor growth, and that YAP/TAZ promoted T cell exclusion by activating tissue remodeling programs with Tgfb2 as a critical target gene. These results support pulsed YAP/TAZ pathway inhibition as a therapeutic approach and link a specific ECM-driving signaling axis (YAP/TAZ→Tgfb2) to immune exclusion.

Jessen M, Kim K, Tollot-Wegner M et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

Tumor cell-derived extracellular vesicles foster the immunosuppressive landscape of pancreatic cancer.

The study tested whether extracellular vesicles (EVs) released by pancreatic ductal adenocarcinoma (PDAC) tumor cells shape the immunosuppressive tumor microenvironment. Using human bone-marrow-derived monocytes and PDAC tumor cells, it showed that tumor cell–derived EVs induced differentiation into M2-like immunosuppressive macrophages characterized by CD200R+/PD-L1+/HLA-DR- and ALOX15b expression, associated with poor prognosis. This demonstrates a mechanism by which tumor EVs actively program macrophage immunosuppression and highlights ALOX15b+ M2-like macrophages as potential therapeutic targets.

Hussain Z, Montenegro C, Rovera C et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

The dual role of mTOR in multiple sclerosis pathophysiology: a systematic review.

This systematic review assessed the mechanistic target of rapamycin (mTOR) signaling pathway’s role in multiple sclerosis (MS) pathophysiology across preclinical and clinical studies. The review concluded that mTOR has a dual role in MS, influencing immune responses, metabolism, autophagy, and repair processes while also contributing to neurodegeneration depending on context and model. Clarifying mTOR’s context-dependent effects is scientifically significant because it informs how mTOR-targeting strategies (eg, rapamycin-pathway modulation) might be optimized for MS treatment.

Koks F, Reubens F, van der Zee H et al. · Journal of neurology · (2026) · View on PubMed ↗

Comorbid autoimmune disease in stiff-person syndrome spectrum disorder: a systematic review and meta-analysis.

This systematic review and meta-analysis quantified the pooled frequency of autoimmune comorbidities in stiff-person syndrome spectrum disorder (SPSD) and compared rates by clinical subtype and by GAD65 antibody status (positive vs negative). Across included studies, autoimmune comorbidities were common in SPSD, with differences observed between GAD65 antibody-positive and -negative groups and among SPSD subtypes. Estimating comorbidity burden is clinically significant because it supports targeted screening and more comprehensive long-term management for patients with SPSD.

Hu Y, Wen M, Wen L et al. · Journal of neurology · (2026) · View on PubMed ↗

A novel dose-dense strategy for CD19-directed CAR T-cell therapy is associated with durable responses without increased toxicity in patients with B-cell non-Hodgkin lymphoma.

This phase 1/2 trial pilot cohort tested a novel dose-dense strategy for CD19-directed CAR T-cell therapy in patients with relapsed/refractory B-cell non-Hodgkin lymphoma (B-NHL), using a second infusion at day 14 at the same JCAR014 dose (2×10^6 CAR+ cells/kg) without repeat lymphodepletion. The dose-dense approach was associated with durable responses without increased toxicity compared with expectations from standard single-infusion strategies. These findings suggest that schedule optimization (dose-dense re-dosing) can improve efficacy while maintaining safety in CD19 CAR T-cell therapy for B-NHL.

Ortiz-Maldonado V, Liang EC, Huang JJ et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

Favorable tolerability of asciminib versus ATP-competitive tyrosine kinase inhibitors in the ASC4FIRST study of newly diagnosed patients with chronic-phase chronic myeloid leukemia.

This exploratory post-hoc analysis of the phase 3 randomized ASC4FIRST study compared tolerability of asciminib versus ATP-competitive tyrosine kinase inhibitors (specifically imatinib and second-generation TKIs) in newly diagnosed chronic-phase chronic myeloid leukemia (CML). Asciminib, an allosteric BCR::ABL1 inhibitor, showed favorable tolerability with fewer or less burdensome adverse events affecting daily living and treatment persistence. The tolerability advantage supports asciminib as a patient-centered first-line option for newly diagnosed CP-CML.

Issa GC, Larson RA, Hughes TP et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

Female sex is associated with superior outcomes in patients treated with CD19-directed CAR T-cell therapy for large B-cell lymphoma.

This study evaluated whether sex influences outcomes in patients treated with CD19-directed CAR T-cell therapy for large B-cell lymphoma. Female sex was associated with superior treatment outcomes compared with male patients in this CAR T-cell population. The finding may inform risk stratification and future analyses of CAR T-cell response differences by patient sex.

Behman J, Ahmed N, Hashmi S et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

CX3CR1 and CCR2: dynamic myeloid cell states across inflammatory diseases with implications for oral health and disease.

This review summarized evidence on how the chemokine receptors CX3CR1 and CCR2 define dynamic myeloid cell states across inflammatory diseases, emphasizing recruitment-to-residency transitions rather than fixed cell subsets. It highlights CCR2-driven inflammatory monocyte recruitment and CX3CR1-mediated tissue macrophage retention as context-dependent regulators of chronic inflammation. The synthesis has implications for understanding inflammatory pathogenesis and for translational relevance to oral health and disease.

Lim YJ, Kim TS · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

---

Cancer Cell-Intrinsic Signaling & Metabolism

Lipid droplets promote aberrant liquid-liquid phase separation of alpha-synuclein impairing energy homeostasis.

This study tested whether lipid droplets trigger aberrant liquid–liquid phase separation of alpha-synuclein (αSyn) and assessed consequences for cellular energy and lipid homeostasis. It found that lipid droplets promote spontaneous phase separation of wild-type and E46K mutant αSyn into condensates that sequester lipid droplets and impair their turnover, disrupting lipid homeostasis and affecting nearby mitochondria. The results support a mechanistic link between lipid droplet biology, αSyn condensate formation, and metabolic dysfunction relevant to Parkinson’s disease pathology.

Cevallos J, Eubanks E, Jung S et al. · EMBO reports · (2026) · View on PubMed ↗ · Free PDF ↗

BRG1-mediated suppression of ferroptosis underlies BTK inhibitor resistance.

This study investigated mantle cell lymphoma (MCL) resistance to Bruton’s tyrosine kinase inhibitors (BTKi) and the role of the chromatin remodeler BRG1 in regulating ferroptosis. BRG1 promoted BTKi resistance by inducing a BTK-dependent survival program and a BTK-independent transcriptional program centered on MEF2B, which upregulated the atypical mitochondrial complex I subunit N and restricted ROS and labile iron to suppress ferroptosis. Clinically, targeting the BRG1–MEF2B axis may help overcome ferroptosis-based vulnerabilities that drive BTKi treatment failure in B-cell malignancies.

Hwang SY, Huang X, Nikolli H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

A ZDHHC3-USP5-PTRF axis links palmitoylation to ferroptosis-associated phenotypes in melanoma.

This study investigated how the ZDHHC3–USP5–PTRF signaling axis links palmitoylation-related regulation to ferroptosis-associated phenotypes in melanoma using proteomic, biochemical, and functional approaches. USP5 was upregulated in melanoma and promoted proliferation, migration, and invasion by directly interacting with PTRF and deubiquitinating it, preferentially removing K48-linked polyubiquitin chains to reduce proteasomal degradation. By defining USP5 as a regulator of PTRF stability tied to ferroptosis-associated behavior, the study highlights a potential molecular target for improving melanoma therapeutic responses.

Zhao S, Liu Y, Wu D et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

TERT drives liver tumorigenesis beyond telomere elongation.

This study used two genetically engineered mouse models (p21+/Tert and p21+/TertCi) to test whether telomerase reverse transcriptase (TERT) drives liver tumorigenesis beyond telomere elongation. Both models developed liver tumors with human hepatocellular carcinoma–like histopathology, but the mutational spectra differed by telomerase activity status (Ctnnb1 and PP1 alterations in Tert-active tumors versus HrasGln61Lys with elevated C>A transversions in TertCi tumors). The results indicate that TERT can promote liver cancer through telomere-independent mechanisms, informing how telomerase-targeted strategies might be combined or refined.

Braud L, Vernerey J, Guille A et al. · Life science alliance · (2026) · View on PubMed ↗ · Free PDF ↗

USP20 promotes CD8+ T cell exhaustion and impairs KRASG12D inhibitor efficacy by orchestrating cholesterol metabolism and autophagy in pancreatic cancer.

This study investigated how USP20 regulates CD8+ T cell exhaustion and reduces efficacy of KRASG12D inhibitor therapy in pancreatic ductal adenocarcinoma (PDAC) by integrating whole-exome sequencing, untargeted metabolomics, and single-cell RNA sequencing of human tumor specimens. USP20 promoted CD8+ T cell exhaustion and impaired KRASG12D inhibitor response by orchestrating tumor cholesterol metabolism and autophagy programs that shape the immunosuppressive microenvironment. These findings provide a mechanistic rationale for combining KRASG12D inhibitors with strategies targeting USP20-linked metabolic/autophagy pathways to improve immunotherapy responsiveness.

Yu Z, Qing H, Wang T et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗

Extracellular ATP-P2RY2 signaling drives intratumoral prostaglandin E2 accumulation and adaptive resistance to immunotherapy in solid tumors.

In solid tumor models, the study investigated how extracellular ATP (eATP) signaling through the purinergic receptor P2RY2 in tumor cells drives intratumoral prostaglandin E2 (PGE2) accumulation and adaptive resistance to immunotherapy. eATP increased during immunotherapy, and eATP–P2RY2 signaling induced COX-1/COX-2 expression leading to higher PGE2; genetic deletion or pharmacologic inhibition of P2RY2 reduced baseline and therapy-induced PGE2, altered the tumor immune infiltrate, and improved immunotherapy responsiveness. This identifies a tumor-intrinsic eATP–P2RY2–COX–PGE2 axis as a targetable mechanism of immunotherapy resistance.

Hu Z, Matsuo H, Du S et al. · Immunity · (2026) · View on PubMed ↗ · Free PDF ↗

TMED9 drives non-small-cell lung cancer progression via promotion of autophagy by recruiting USP5 to deubiquitinate ATG9A.

This study examined the role of TMED9 in non-small-cell lung cancer (NSCLC) progression and identified a mechanism involving autophagy regulation. TMED9 was overexpressed in NSCLC and promoted proliferation, invasion, and metastasis, acting by recruiting USP5 to deubiquitinate ATG9A and thereby enhance autophagy. These findings nominate the TMED9–USP5–ATG9A axis as a potential therapeutic target to suppress NSCLC aggressiveness.

Liu N, Han G, Zhang F et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Local signals, systemic decline.

This Science commentary discussed how local tumor-to-nerve signaling induced by a high-fat diet can promote cachexia in mice, linking systemic decline to neural interactions. The central claim is that dietary fat alters tumor–nerve communication, contributing to cachexia development. The significance is that it frames cachexia as a modifiable neurobiological process influenced by diet, suggesting new avenues for preventing or treating cancer-associated wasting.

Gültekin Y, Vander Heiden MG · Science (New York, N.Y.) · (2026) · View on PubMed ↗

A dietary switch promotes sensory neuron-dependent cancer-associated cachexia.

The study tested how dietary changes affect cancer-associated cachexia mechanisms in preclinical lung cancer models, focusing on tumor genetics and local inflammatory mediators. It found that loss of Lkb1 promotes cachexia and that an obesogenic high-fat diet worsened sickness, with tumor-derived local prostaglandin E2 (PGE2) driving sickness and cachexia that was suppressed by genetic, dietary, and pharmacological inhibition of tumor PGE2. It also showed that abrogating lung sensory neurons prevents the sickness/catabolic phenotype, highlighting a tumor–PGE2–sensory neuron axis as a therapeutic target.

Cross M, Kotschi S, Wu W et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗

CDK2 Inhibition Exerts RB-Independent Antitumor Activity in CDK4/6 Inhibitor-Resistant HR+/HER2- Breast Cancer.

The study analyzed tumor and liquid biopsies from patients with CDK4/6 inhibitor-resistant HR+/HER2- metastatic breast cancer treated with the selective CDK2 inhibitor PF-07104091. It found that PF-07104091 monotherapy produced disease stabilization with responses occurring regardless of RB expression and phosphorylation status. This supports RB-independent antitumor activity of CDK2 inhibition as a potential therapeutic strategy for CDK4/6i-resistant breast cancer.

Juric D, Islam KN, Gkotinakou IM et al. · Cancer research · (2026) · View on PubMed ↗ · Free PDF ↗

Targeted Delivery of Indole-3-Pyruvic Acid Suppresses Macrophage Ferroptosis to Enhance CD8+ T Cell-Mediated Immunotherapy Response in Bladder Cancer.

The study evaluated whether targeted delivery of indole-3-pyruvic acid (I3P) can suppress macrophage ferroptosis to improve CD8+ T cell–mediated immunotherapy in bladder cancer. Mechanistically, I3P acted through an AHR–NF-κB–SLC7A11 signaling axis to maintain macrophage redox homeostasis, suppress ferroptosis, and sustain CD8+ T cell activity, with disruption of AHR or NF-κB abolishing the effects. The therapeutic significance is that liposomal I3P delivery preferentially targets tumor-associated macrophages and enhances immunotherapy response, suggesting a metabolite-based adjuvant strategy.

Lao J, Yuan X, Liang S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Identification of PRKCB, NLRC4, and TNFSF10 as Key Regulators of the Lipid Metabolism-Autophagy Network in Atherosclerosis.

This study integrated bulk transcriptome and single-cell RNA sequencing data from atherosclerosis to identify lipid metabolism–autophagy regulatory genes, using WGCNA and LASSO regression to pinpoint key regulators including PRKCB, NLRC4, and TNFSF10. PRKCB, NLRC4, and TNFSF10 emerged as central regulators of a lipid metabolism–autophagy network, linking immune-related pathways to autophagy and lipid dysregulation in atherosclerotic contexts. These findings suggest PRKCB/NLRC4/TNFSF10 as candidate therapeutic targets or biomarkers for modulating autophagy–lipid crosstalk in atherosclerosis.

Li M, Sun Y, Sun Y et al. · Cell biochemistry and function · (2026) · View on PubMed ↗

Mitochondrial STING Governs Glycolytic Reprogramming in Diabetic Cardiomyopathy.

This study investigated how mitochondrial STING regulates glycolytic reprogramming in diabetic cardiomyopathy using genetic (db/db) and chemically induced (high-fat diet plus streptozotocin) diabetic mouse models. Using single-cell RNA sequencing, echocardiography, and transmission electron microscopy, the authors found that mitochondrial STING governs metabolic remodeling toward glycolysis in the diabetic heart. Mechanistically targeting STING-mediated metabolic reprogramming could represent a therapeutic strategy to prevent or reverse diabetic cardiac dysfunction.

Zhang S, Zhao D, Wang M et al. · Circulation research · (2026) · View on PubMed ↗

Metabolic Dysfunction-Associated Fatty Liver Disease: From Pathogenesis to Treatment.

This review summarized current understanding of metabolic dysfunction-associated fatty liver disease (MAFLD) pathogenesis and treatment, focusing on mechanisms linking obesity and insulin resistance to progressive liver injury. It highlights dysregulated lipid metabolism, mitochondrial dysfunction, oxidative stress, inflammatory signaling, bile acid imbalance, and gut microbiota-derived metabolites as drivers from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. By integrating pathogenesis with therapeutic directions, the review supports more targeted treatment strategies for a leading global chronic liver disease.

Cui Z, Du X, Amevor FK et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

---

DNA Replication, Genome Stability & Cell Cycle

TTF2 processes sites of incomplete DNA replication during mitosis via sister-chromatid exchanges.

The study investigated how cells process incomplete DNA replication during mitosis to enable chromosome segregation, focusing on the TRAIP ubiquitin ligase pathway. It found that the TTF2 ATPase acts as a phospho-receptor binding a conserved phosphorylation site on TRAIP during mitosis, coupling phosphorylated TRAIP to DNA polymerase epsilon (Pol ε) to drive TRAIP ubiquitylation of the CMG helicase (CDC45–MCM–GINS) and thereby promote processing of cleaved replication forks. This clarifies a mechanistic link between mitotic fork cleavage and replisome/chromosome segregation, identifying TTF2 as a key regulator of incomplete replication handling.

Fujisawa R, Labib KPM · Science (New York, N.Y.) · (2026) · View on PubMed ↗

A CDK1 phospho-switch reprograms TRAIP to unload replisomes in mitosis.

The study investigated how the CDK1 phospho-switch reprograms the replisome-associated E3 ubiquitin ligase TRAIP during mitosis in cells entering mitosis with incompletely replicated DNA. Key findings were that TTF2 recruits Cyclin B–CDK1-phosphorylated TRAIP to the replisome, switching TRAIP from trans-acting to cis-acting ubiquitylation to promote replisome disassembly, fork breakage, and joining of broken chromosome arms. This mechanism explains how mitotic cells process unreplicated DNA to prevent catastrophic chromosome segregation failure and identifies a potential target axis (TTF2–CDK1–TRAIP) for controlling genome instability.

Can G, Shyian M, Krishnamoorthy A et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

---

Epigenetics & Chromatin Regulation

A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.

This review synthesizes genomic and epigenomic profiling findings in acute lymphoblastic leukemia (ALL), focusing on how molecular subtypes refine classification beyond traditional immunophenotyping. It highlights that B-cell precursor ALL (B-ALL) has been subdivided into many genetically defined groups with distinct transcriptional programs and regulatory alterations, while T-cell ALL (T-ALL) is increasingly being reclassified into biologically defined genomic subtypes. The clinical significance is improved risk stratification, therapeutic decision-making, and disease monitoring driven by molecular taxonomy.

Iacobucci I, Mullighan CG · Nature reviews. Cancer · (2026) · View on PubMed ↗

Histone lactylation-driven IGF2BP3 promotes intrahepatic cholangiocarcinoma progression via SPP1/CD44-dependent macrophage polarization.

This study investigated how histone lactylation at H3K18 (H3K18la) regulates IGF2BP3 transcription in intrahepatic cholangiocarcinoma and how this drives tumor–macrophage communication. Using CUT&Tag/Cleavage Under Target and Tagmentation, it showed H3K18la enrichment at the IGF2BP3 promoter, promoting IGF2BP3-dependent progression via an SPP1/CD44-dependent macrophage polarization axis. The findings connect a specific epigenetic modification (H3K18la) to macrophage reprogramming through IGF2BP3 and SPP1/CD44 signaling, identifying potential therapeutic targets in the tumor microenvironment.

Lang Q, Yin Z, Sun J et al. · Oncogene · (2026) · View on PubMed ↗

Kat5 deficiency in alveolar type II cells licenses STAT6-driven glycolytic reprogramming and pulmonary fibrosis.

This study used Kat5-deficient models in alveolar type II (ATII) cells to define how epigenetic regulation controls fibrotic progression in pulmonary fibrosis. It found that Kat5 acetylates STAT6 at lysine 636 (K636) to suppress STAT6 dimerization, phosphorylation, and nuclear translocation, and that reduced STAT6 acetylation in fibrotic lungs enables STAT6-driven glycolytic reprogramming via hexokinase 2 (HK2) transcription. The significance is identification of a Kat5–STAT6–HK2 metabolic axis as a driver of pulmonary fibrosis and a potential target for therapeutic intervention.

Yang Y, Ling Y, Li J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Surface immune signaling unlocks NLR activation through mRNA alternative splicing.

The study investigated how surface immune signaling coordinates plant nucleotide-binding leucine-rich repeat (NLR) activation while preventing autoimmunity. It found that pathogen-triggered PTI induces alternative mRNA splicing of the potato late blight resistance gene Rpi-vnt1.1, where an N-terminal prodomain normally inhibits resistosome formation and splicing removes this inhibition to unlock NLR activation. This reveals a splicing-based safety switch linking pattern-triggered immunity to controlled NLR function.

Gao C, Meng X, Chen X et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

---

Protein Engineering, Structural Biology & Biophysics

The Target ALS Global Natural History Study: Cross-platform proteomics to accelerate biofluid biomarker and drug target discovery in amyotrophic lateral sclerosis.

This cross-platform proteomics study used 35-plex TMTpro (isobaric tandem mass tag) labeling to profile cerebrospinal fluid (CSF) and plasma from controls and sporadic ALS (sALS) participants in the Target ALS Global Natural History Study (TALS GNHS). It identified thousands of proteins (2,875 in CSF; 1,118 in plasma) and reported known and novel differentially expressed proteins between controls and sALS. These biomarker and drug-target discovery candidates could accelerate development of ALS diagnostics and therapeutics by leveraging unbiased proteomic signatures.

Yasui D, Weatherill D, Dugom L et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Cell surface liposome binding (CLiB) allows lipid-binding probe engineering via high-throughput screening.

This work developed the cell surface liposome binding (CLiB) assay to engineer lipid-binding protein domains and applied it to directed evolution of the PX domain from SnxA in cells. Using CLiB with next-generation sequencing, the authors isolated high-affinity SnxA PX variants specific for phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2) and screened >6,000 clones in parallel. The method provides a general, high-throughput platform for creating tailored lipid probes to study membrane lipid dynamics and compartmentalization.

Nishimura T, Tsuboyama K, Nakagaki Y et al. · Nature cell biology · (2026) · View on PubMed ↗

Membrane protein solubilization and structure determination using de novo-designed proteins.

The study developed a deep learning-based protein design strategy to solubilize and determine structures of native integral membrane proteins using genetically encoded de novo proteins. It found that designed water-soluble RFdiffused amphipathic proteins (WRAPs) can surround hydrophobic surfaces of both beta-barrel outer membrane proteins and helical multipass proteins to preserve sequence, fold, active sites, and ligand-binding while enabling thermostable, detergent-free solubilization. This provides a general platform to accelerate structural biology and therapeutic/vaccine development against difficult membrane protein targets.

Mihaljević L, Kim DE, Bandawane PD et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

Nanoscale morphological and structural analysis of round and donut oligomers formed by C-terminal domain of TDP-43.

This physical chemistry study used nanoscale morphological and structural characterization methods to analyze round and donut oligomers formed by the C-terminal domain (CTD) of TDP-43. The authors found distinct oligomer morphologies consistent with CTD-driven self-assembly into different nanoscale structures, supporting the CTD as a key trigger of pathological aggregation. Understanding the structure of TDP-43 oligomers is clinically significant for ALS/FTD biology because it can inform how toxic species form and potentially guide strategies to detect or disrupt early aggregation intermediates.

Pickett D, Purvinsh Y, Skrehot JT et al. · Physical chemistry chemical physics : PCCP · (2026) · View on PubMed ↗ · Free PDF ↗

---

CRISPR & Genetic Engineering (Host/Parasite/Prokaryote)

An assay to quantify sexual commitment and stage conversion in the human malaria parasite Plasmodium falciparum.

This Nature Protocols update presents an assay to quantify sexual commitment and stage conversion rates in the human malaria parasite Plasmodium falciparum during the blood stage. It combines three previously validated tools using standardized minimal medium to reproducibly track conversion from asexual replicative schizont stages to sexual gametocyte stages. The assay enables more precise measurement of transmission-relevant differentiation, supporting research on malaria biology and evaluation of interventions targeting sexual development.

Venugopal K, Borbon EDA, Thommen BT et al. · Nature protocols · (2026) · View on PubMed ↗

Prokaryotic Schlafen proteins cleave tRNAs during type III CRISPR immunity.

This study investigated prokaryotic CRISPR-associated Schlafen (Cash) proteins in Chloroflexi bacterium, focusing on how a Schlafen domain fused to Csx15 responds to cyclic tetra-adenylate (cA4) during type III CRISPR interference. Cash was activated by cA4 to form an aligned filament that enables catalytic interface formation, inducing cell toxicity primarily by cleaving tRNAs at the T-loop. These findings reveal a mechanistic link between type III CRISPR signaling and tRNA-targeted nuclease defense, expanding Schlafen biology beyond mammalian self-RNA cleavage.

Weickert P, Liu Y, Strecker J · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Meiotic cohesin Rec8 imposes fitness costs on fission yeast gametes favoring the evolution of parental bias in gene expression.

The study investigated how meiotic cohesin Rec8 affects fitness costs in fission yeast gametes and how this can drive evolution of parental bias in gene expression. In Schizosaccharomyces pombe, P- and M-type partner gametes—morphologically identical—contributed different amounts of conserved meiotic cohesins, leading to asymmetric zygotic development and selection for parental bias. This mechanistic work links Rec8-dependent gamete/zygote fitness differences to non-Mendelian inheritance patterns, informing theories of sex evolution and gene-expression asymmetry.

Martins C, Booth H, Salat-Canela C et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Manipulation of protein translation and stem cell self-renewal by CRISPR activation of rRNA transcription.

The study developed TAPIR, a CRISPR activation strategy that targets 47S rDNA transcription to manipulate rRNA levels and thereby protein translation in rapidly proliferating cells and neural stem cells. TAPIR increased nucleolar size and protein synthesis and, in neural stem cells, enhanced self-renewal and proliferation both in vitro and in vivo. These results establish CRISPR activation of rRNA transcription as a tunable lever for stem-cell biology and provide a platform to model and partially rescue rRNA dysregulation–associated diseases.

Wiesbeck M, Alard EL, Merino F et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neurobiology, Brain Circuits & Biomarkers

Sparse component analysis: A method that uncovers separable computations within neural population activity.

This paper introduced sparse component analysis (SCA), an unsupervised method designed to uncover separable latent computations within neural population activity. Applied to motor cortex activity during reach behavior, SCA produced clear parcellations of neural activity using both linear and nonlinear embeddings without requiring supervision. The method provides a new computational tool for discovering how brain circuits implement multiple distinct computations from population dynamics.

Zimnik AJ, An X, Ames KC et al. · Neuron · (2026) · View on PubMed ↗

Sub-second fluctuations between top-down and bottom-up modes distinguish diverse human brain states.

The study examined human brain state dynamics using electroencephalography (EEG) and a newly introduced relative phase analysis (RPA) method to quantify millisecond-scale information flow between top-down and bottom-up modes. RPA detected sub-second alternations occurring about every 200 ms between two dominant whole-brain information modes. This provides a high-temporal-resolution framework to distinguish neurocognitive and neuropsychiatric brain states beyond second-scale fMRI, potentially improving mechanistic biomarkers of consciousness and cognition.

Park Y, Cha Y, Kim H et al. · Current biology : CB · (2026) · View on PubMed ↗

Fruit flies actively restart their circadian clock by proactively shaping their environment.

The study investigated how fruit flies maintain or restart circadian rhythms when exposed to constant illumination by actively shaping their environment. It found that light-induced degradation of the core clock protein Timeless stops rhythms, but flies can regain rhythmic locomotion by choosing to move between dark and illuminated areas in constant light, accompanied by molecular rhythms in clock neurons. This demonstrates an adaptive, behavior-driven mechanism for circadian clock recovery that extends beyond purely molecular clock resetting.

Coculla A, Garcia Rodriguez L, Ogueta M et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

---

Neurodevelopment & Cortical Development

SMPD4 deficiency disrupts indirect neurogenesis and neuronal migration in gyrencephalic cortex.

This study investigated how SMPD4 loss affects cortical development by using in utero electroporation with CRISPR-Cas9 genome editing to knock out Smpd4 in a gyrencephalic cortex model. SMPD4 deficiency disrupted indirect neurogenesis and neuronal migration, producing cortical developmental abnormalities that better align with human SMPD4-related neurodevelopmental phenotypes than prior mouse models. Creating a gyrencephalic, gene-edited model is scientifically significant because it enables mechanistic dissection of SMPD4-driven cortical pathology and helps reconcile species-specific differences.

Wang CX, Yang FW, Zhao MM et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗

---

Infectious Disease & Viral Immune Evasion

A viral ORFeome library for systems-level genetic dissection of host-pathogen interactions.

Researchers developed a barcoded viral ORFeome library containing ~12,000 viral open reading frames (vORFs) from 513 viral species to systematically dissect host–pathogen interactions. Using pooled functional screens, they identified hundreds of viral regulators of cellular proliferation, MHC class I antigen presentation, and interferon signaling, and then characterized two previously uncharacterized viral proteins (MC162R and Yaba-like disease–associated protein). This systems-level genetic approach expands the functional virome map and enables targeted mechanistic studies of viral immune evasion and host control.

Fujimura E, O’Leary CN, Li MZ et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

Tegument protein UL16 of herpes simplex virus 1 suppresses the innate immune response by downregulating MAVS abundance via mitophagy.

The study examined how the HSV-1 tegument protein UL16 modulates innate antiviral signaling in the context of RIG-I-like receptor (RLR) immunity. UL16 suppressed type I interferon production by interacting with MAVS and inducing its degradation via mitophagy, thereby reducing MAVS abundance and dampening RLR-mediated antiviral responses. This identifies a viral immune-evasion mechanism (UL16–MAVS–mitophagy) that could inform antiviral strategies targeting host-pathway steps.

Wang J, Zhu R, Yi P et al. · Autophagy · (2026) · View on PubMed ↗

---

Cardiovascular Disease (Clinical Trials/Guidelines/Diagnostics)

Frailty as a predictor of adverse in-hospital outcomes in older patients with Takotsubo cardiomyopathy.

This retrospective study examined whether frailty predicts adverse in-hospital outcomes in older adults (age ≥65) hospitalized with Takotsubo cardiomyopathy (TCM) using the National Inpatient Sample (2016–2021). Frailty was defined using Johns Hopkins ACG frailty-defining diagnoses, and its association with outcomes was evaluated with multivariable analyses. The findings support frailty stratification as a clinically useful risk marker to anticipate complications and guide management in elderly TCM patients.

Bahar AR, Bahar Y, Sirekulam V et al. · Journal of geriatric cardiology : JGC · (2026) · View on PubMed ↗

Pulsed Field Ablation With a Variable Loop Circular Catheter in Atrial Fibrillation: Acute Outcomes From the VARIPURE Multicenter Study.

The VARIPURE multicenter observational SECURE postmarket follow-up substudy evaluated acute safety and effectiveness of first-time pulmonary vein isolation using a variable loop circular catheter (VLCC) pulsed field ablation (PFA) in patients with atrial fibrillation undergoing standard clinical practice. Acute procedural success and primary adverse events related to the VLCC/PFA system were assessed from electronic data capture and analytics tools. This provides real-world evidence on the immediate performance of VLCC-PFA for AF, supporting clinical adoption and refinement of PVI workflows.

Almorad A, Sebag FA, Kronborg MB et al. · Heart rhythm · (2026) · View on PubMed ↗ · Free PDF ↗

Consensus Guidelines for Therapeutic Drug Monitoring in Neuropsychopharmacology: Update 2026 - Pharmacokinetic, pharmacogenetic and clinical aspects.

This 2026 consensus guideline update from the AGNP-TDM task force synthesized evidence to revise therapeutic drug monitoring (TDM) reference ranges and dose-related reference ranges across neuropsychopharmacology. The key update is a transparent, systematic methodological approach for determining therapeutic and dose-related ranges for each substance, incorporating pharmacokinetic, pharmacogenetic, and clinical considerations. Clinically, it standardizes how clinicians interpret blood levels to personalize psychiatric/neurologic pharmacotherapy and improve safety and efficacy.

Hart XM, Gründer G, Hiemke C et al. · Pharmacopsychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Temozolomide Versus Radiotherapy as First-Line Therapy for Low-Grade Glioma: Mature Results of a Randomized Phase III Trial (EORTC 22033-26033/NCIC-CTG/TROG/MRC-CTU).

This randomized phase III trial compared dose-dense temozolomide (TMZ) versus standard radiotherapy (RT) as first-line therapy in 478 patients with clinical high-risk WHO grade 2 low-grade glioma (EORTC 22033-26033/NCIC-CTG/TROG/MRC-CTU). Mature results showed no significant difference in progression-free survival or overall survival between TMZ and RT. Scientifically and clinically, it supports RT as an equivalent standard option to TMZ for high-risk LGG while informing how molecular markers may be used to refine future treatment selection.

Baumert BG, Hegi ME, van den Bent MJ et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · 1 citations · View on PubMed ↗

Cardiac Risk After Heart-Sparing Breast Radiotherapy.

This cross-sectional study compared radiation dose metrics—whole-heart versus left anterior descending coronary artery (LAD) dose—to predict cardiac risk after heart-sparing breast radiotherapy. It included breast cancer patients treated with 3D conformal or intensity-modulated radiotherapy from 2008 to 2018 and evaluated which dosimetric approach better captured subsequent cardiac risk. The significance is that it tests whether LAD-focused planning metrics improve cardiac risk prediction, potentially guiding radiotherapy planning to reduce long-term cardiovascular toxicity.

Quirk S, Atkins KM, Logie N et al. · JAMA oncology · (2026) · View on PubMed ↗

Prehospital airway and ventilatory management: a collaborative and narrative review.

This collaborative narrative review synthesized evidence on prehospital airway and ventilatory management, focusing on techniques such as prehospital tracheal intubation and non-invasive ventilation/high-flow nasal oxygen across different emergency care systems. It highlighted best-practice elements including appropriate indications, timing, physiologic optimization, procedural conduct, and post-intubation management to reduce high-stakes complications. Standardizing evidence-based prehospital ventilation and airway approaches is clinically significant because it can improve patient outcomes despite variability in provider training and system design.

Vieux T, Marjanovic N, Ward A Maia I et al. · Intensive care medicine · (2026) · View on PubMed ↗

Implantable Cardioverter-Defibrillator Therapy in Contemporary Heart Failure Patients: An Analysis From the EMPEROR-Reduced Trial.

This analysis of the EMPEROR-Reduced trial evaluated the impact of implantable cardioverter-defibrillator (ICD) therapy in contemporary heart failure with reduced ejection fraction (HFrEF) patients receiving foundational therapy that included an SGLT2 inhibitor (empagliflozin). Using propensity score matching and Cox regression/time-to-event methods, the study compared outcomes between participants with vs without an ICD within the placebo and empagliflozin arms. Determining whether ICD benefit persists in the SGLT2 inhibitor era is clinically significant for guiding device decisions in modern HFrEF care.

Aktaş MK, Talha KM, Goldenberg I et al. · JACC. Heart failure · (2026) · View on PubMed ↗

ACG Clinical Guideline: Colonic Diverticulitis.

This ACG Clinical Guideline summarized evidence-based recommendations for outpatient management of colonic diverticulitis, including diagnosis, clinical course, antibiotic use, and prevention. It emphasized that computed tomography (CT) imaging is essential to confirm diverticulitis—especially at first presentation and in severe cases—and that colonoscopy is recommended after complicated diverticulitis and suggested after uncomplicated disease with alarm symptoms. Providing standardized diagnostic and follow-up pathways is clinically significant because it can reduce unnecessary antibiotics, improve diagnostic accuracy, and optimize surveillance after recovery.

Peery AF, Strate LL, Stollman N et al. · The American journal of gastroenterology · (2026) · View on PubMed ↗

Management of Patients at Risk of Ischemic Stroke With Left Ventricular Systolic Dysfunction in the Absence of Intracardiac Thrombus: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement reviewed evidence for managing patients with ischemic stroke who have left ventricular (LV) systolic dysfunction (ejection fraction ≤40% or wall motion abnormality) but no intracardiac thrombus. It concludes that incident and recurrent embolic stroke risk is increased in this population while acknowledging that direct evidence supporting anticoagulation is limited, and it provides best-practice recommendations based on available data and a narrative summary plus meta-analysis of secondary analyses. The guidance is intended to standardize post-stroke management decisions for patients with LV dysfunction without detected thrombus.

Sharma R, Levine GN, Spinler SA et al. · Stroke · (2026) · View on PubMed ↗

Hypoxia-Induced Epas1-Myl9/12 Axis Shapes the Pathology of Pulmonary Hypertension.

The study investigated how hypoxia regulates the Epas1–Myl9/12 signaling axis in a Sugen/hypoxia mouse model of pulmonary hypertension, focusing on Myl (myosin light chain) 9/12–driven vascular remodeling. Hypoxia induced an Epas1-dependent Myl9/12 pathway that shaped pulmonary hypertension pathology, including vascular changes consistent with endothelial dysfunction and smooth muscle remodeling. These mechanistic findings identify the Epas1–Myl9/12 axis as a potential therapeutic target to prevent or modify hypoxia-driven pulmonary vascular disease.

Kuriyama S, Iwamura C, Kiuchi M et al. · Circulation research · (2026) · View on PubMed ↗

Effects of Acoramidis on Kidney Function in Transthyretin Amyloid Cardiomyopathy.

The study analyzed kidney function effects of acoramidis in patients with transthyretin amyloid cardiomyopathy using pooled data from randomized phase 2 (N=49) and phase 3 (N=632) trials. Acoramidis was associated with measurable longitudinal changes in eGFR slope and urinary albumin-to-creatinine ratio, and these kidney-function trajectories were evaluated for links to clinical outcomes using Cox models. Clarifying acoramidis’ renal impact is clinically important for optimizing long-term management of transthyretin amyloid cardiomyopathy beyond cardiovascular hospitalization reduction.

Testani JM, Judge DP, Borlaug BA et al. · Circulation. Heart failure · (2026) · View on PubMed ↗

---

Thrombosis & Anticoagulation (Clinical Evidence)

Apixaban for the treatment of venous thromboembolic events in paediatric patients: an open-label, multicentre, randomised, controlled descriptive trial.

In a prospective, open-label, multicentre, randomized controlled descriptive trial conducted across 120 sites in 14 countries, investigators studied apixaban for treatment of venous thromboembolic events in pediatric patients. The trial assessed safety and efficacy over a 12-week main treatment phase with an optional 6–12-week extension for patients requiring continued anticoagulation. This addresses a major evidence gap by generating direct clinical data to guide DOAC use for pediatric VTE management.

Brandão LR, Driscoll J, Newburger JW et al. · The Lancet. Haematology · (2026) · 1 citations · View on PubMed ↗

Incidence and predictors of recurrent venous thromboembolism after isolated distal deep vein thrombosis: a post-hoc analysis of the RIDTS trial.

This post-hoc analysis of the RIDTS randomized, double-blind trial evaluated incidence and predictors of recurrent venous thromboembolism (VTE) after stopping anticoagulation in patients with isolated distal deep vein thrombosis (IDDVT) without cancer, comparing 6 vs 12 weeks of rivaroxaban. Among 398 participants, 15.3% experienced recurrent VTE after treatment cessation (median 6.2 months), with most recurrences being recurrent IDDVT and a smaller fraction proximal DVT or symptomatic pulmonary embolism. Identifying predictors of recurrence after rivaroxaban cessation can help refine duration-of-therapy decisions for IDDVT patients.

Potere N, Bertù L, Bucherini E et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

Bleeding Risk With Apixaban Versus Rivaroxaban: A Reference Trial Emulation Predicting the Results of COBRRA-VTE and COBRRA-AF Using US Health Care Claims.

The study emulated the ongoing COBRRA-VTE and COBRRA-AF randomized trial designs using US health care claims to compare bleeding risk between apixaban and rivaroxaban in patients with venous thromboembolism and atrial fibrillation. Using reference-trial emulation methods, it aimed to predict the comparative bleeding outcomes that the COBRRA trials are designed to measure. This approach supports evidence generation for DOAC safety in real-world populations and can inform anticoagulant selection when head-to-head trial results are pending.

Mahesri M, Schneeweiss S, Lin KJ et al. · Circulation. Population health and outcomes · (2026) · 1 citations · View on PubMed ↗

---

Oncology Diagnostics, Imaging & Risk Stratification

Signaling Mutations Negate the Favorable Impact of NPM1 Mutations in Older Patients With Newly Diagnosed Acute Myeloid Leukemia Treated With VEN/HMA.

This study evaluated how signaling gene (SG) mutations modify prognosis in older patients with newly diagnosed acute myeloid leukemia (AML) carrying NPM1 frameshift mutations treated with venetoclax plus hypomethylating agents (VEN/HMA). It found that the favorable impact typically associated with NPM1mut is negated when NPM1mut co-occurs with SG mutations under ELN 2024 risk logic, using two independent patient cohorts for validation. Clinically, this supports more accurate risk stratification and treatment planning for NPM1-mutant AML by incorporating co-mutation status with SGs.

Hoff FW, Zeidner JF, Torlapati G et al. · American journal of hematology · (2026) · View on PubMed ↗ · Free PDF ↗

BoneCoT: multicentre validation of a whole-body skeleton foundation model for bone metastases guided by clinician-derived chain of thought.

This multicentre study evaluated BoneCoT, a whole-body skeleton foundation model that integrates clinician-derived chain-of-thought to guide interpretation of CT images for bone metastases. It addresses diagnostic discrepancies among radiologists, pathologists, and oncologists by validating an automated system intended to deliver expert-level predictions using multidisciplinary information. If validated broadly, BoneCoT could standardize bone-metastasis assessment and reduce inter-specialist variability in routine clinical workflows.

Zhao H, Zhang R, Wang Z et al. · Nature biomedical engineering · (2026) · View on PubMed ↗

Germline CDK12 variants in aggressive prostate cancer.

This study assessed germline CDK12 variants in aggressive metastatic prostate cancer by analyzing 4,535 tested patients and comparing findings to population controls (gnomAD). Five patients (0.1%) carried germline CDK12 truncating variants, and all had CDK12-driven cancers defined by an additional somatic CDK12 variant and the CDK12-specific hallmark genomic instability signature characterized by hundreds of tandem duplications. The enrichment of germline CDK12 truncations in metastatic prostate cancer (odds ratio 11.4) supports germline testing considerations for patients with CDK12-driven tumor profiles.

Tolmeijer SH, Maurice-Dror C, Sandhu S et al. · Cancer discovery · (2026) · View on PubMed ↗

Molecular Tumor Board-Guided Osimertinib Therapy in EGFR L858R/Q701L-Mutant Lung Adenocarcinoma Supported by Functional Validation.

This case report studied molecular tumor board (MTB)-guided treatment selection using functional validation to support osimertinib therapy in a 59-year-old woman with metastatic EGFR L858R/Q701L-mutant lung adenocarcinoma. The MTB integrated genomic findings with functional evidence to justify osimertinib despite a rare compound EGFR variant with potential resistance implications. Clinically, it supports an MTB-plus-functional-validation approach for optimizing targeted therapy in NSCLC when standard evidence is limited for uncommon EGFR compound mutations.

Albers-Leischner C, Ritgen M, Paulsen FO et al. · The oncologist · (2026) · View on PubMed ↗ · Free PDF ↗

Association of a Polygenic Risk Score with Diagnosis and Outcomes in Idiopathic Pulmonary Fibrosis.

The study evaluated whether a polygenic risk score (PRS) for idiopathic pulmonary fibrosis (IPF) predicts IPF diagnosis and lung transplant-free survival using real-world electronic healthcare record data across four cohorts (Mass General Brigham Biobank, Mayo Clinic Biobank, Mayo Clinic Tapestry, and a UK cohort). The PRS was associated with IPF diagnosis and with transplant-free survival outcomes, demonstrating performance beyond traditional clinical risk assessment. This supports PRS implementation for earlier risk stratification and prognosis in IPF using routinely captured healthcare data.

Kalra SS, Grilli CB, Coombes BJ et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗

Risk Prognostication After Hypomethylating Agents Combined With Venetoclax in AML: The PRISM Risk Model.

The study developed and validated the PRISM Risk Model to predict outcomes in adults with newly diagnosed acute myeloid leukemia (AML) treated with hypomethylating agents plus venetoclax (HMA+VEN). Using a multinational dataset of 2,092 patients and elastic net modeling with internal and external validation cohorts, the model integrated clinical, cytogenetic, and molecular features to improve overall survival risk stratification. This provides a more accurate prognostic tool for selecting and tailoring lower-intensity venetoclax-based therapy in AML.

Lachowiez CA, Zeidner JF, Othman J et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Diagnostic Performance of Prespecified OCT Rules for Glaucomatous Optic Neuropathy in Nonpathologic Myopia.

This multicenter diagnostic study evaluated prespecified optical coherence tomography (OCT) rules for detecting glaucomatous optic neuropathy (GON) in myopic eyes across diverse international populations and OCT devices. The prespecified OCT criteria showed diagnostic performance that addressed the problem of commercial databases misclassifying nonpathologic myopia as abnormal, improving discrimination of GON from myopic structural overlap (eg, optic disc tilt and retinal nerve fiber layer bundle shifts). Standardizing OCT rule-based interpretation in myopia is clinically significant because it can reduce false-positive glaucoma labeling and improve referral and monitoring decisions across settings and device platforms.

Li F, Kong K, Jiang J et al. · JAMA ophthalmology · (2026) · View on PubMed ↗

Circulating Methylated SEPT9 for Detection of Hepatocellular Carcinoma in Cirrhosis.

This prospective cross-sectional diagnostic accuracy study tested whether adding circulating methylated SEPT9 to α-fetoprotein (AFP) improves hepatocellular carcinoma (HCC) detection in patients with cirrhosis undergoing routine surveillance with ultrasonography and AFP at two French academic centers. Methylated SEPT9 provided incremental diagnostic value over AFP alone for identifying HCC during surveillance. Improving noninvasive early detection in cirrhosis is scientifically and clinically important because it targets the current gap in sensitivity for early-stage HCC and could complement imaging-based surveillance.

Oussalah A, Silva Rodriguez M, Conroy G et al. · JAMA oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Long-term follow-up of oral decitabine/cedazuridine plus venetoclax for older or unfit patients with newly diagnosed acute myeloid leukemia.

This single-center phase II study reported long-term follow-up of older or unfit adults with newly diagnosed acute myeloid leukemia (AML) treated with oral decitabine/cedazuridine plus venetoclax, comparing outcomes between de novo and secondary AML. The extended analysis assessed overall response rate, overall survival, relapse-free survival, duration of response, and safety for the frontline cohort receiving decitabine/cedazuridine (35 mg/100 mg on days 1–5) with venetoclax in 28-day cycles. The long-term results support the durability and tolerability of a fully oral decitabine/cedazuridine–venetoclax regimen for patients ineligible for intensive induction.

Htut TW, Kekedjian J, Short N et al. · Haematologica · (2026) · View on PubMed ↗ · Free PDF ↗

From Target Engagement to Treatment Governance: The Evolving Role of Amyloid PET in Anti-Amyloid Therapy.

This article reviewed the evolving role of amyloid PET in anti-amyloid therapy governance for Alzheimer’s disease, focusing on how lecanemab and donanemab shift care from diagnosis to individualized treatment management. It proposes that amyloid PET can quantify target engagement and guide decisions to continue, switch, or discontinue therapy during follow-up within healthcare constraints. The framework is significant for optimizing anti-amyloid treatment exposure while maintaining efficacy and stewardship at the patient level.

Filippi M, Cecchetti G, Ghirelli A et al. · The Lancet regional health. Europe · (2026) · View on PubMed ↗ · Free PDF ↗

---

Lifestyle, Aging, Frailty & Public Health

Risk of Major Malformations Following First-Trimester Exposure to Cariprazine: Preliminary Data From the MGH National Pregnancy Registry for Psychiatric Medications.

This study assessed the risk of major congenital malformations after first-trimester exposure to the atypical antipsychotic cariprazine in pregnant women enrolled in the MGH National Pregnancy Registry for Psychiatric Medications, compared with unexposed psychiatric controls. Preliminary registry data did not show a clear increase in major malformations with cariprazine exposure during the first trimester. These findings provide early, clinically relevant safety information to support risk–benefit discussions for cariprazine use in pregnancy, while highlighting the need for continued prospective follow-up.

Viguera AC, Freeman MP, Slaby EK et al. · Bipolar disorders · (2026) · View on PubMed ↗

Associations of Dietary Patterns and Micronutrients With Major Adverse Cardiovascular Events and Mortality Among Populations With Cardiovascular-Kidney-Metabolic Syndrome Stages 0-3: Results From Two Prospective Cohorts.

This analysis evaluated whether plant-based diet patterns, inflammatory diet scores, and micronutrient intake are associated with major adverse cardiovascular events (MACE) and mortality across cardiovascular-kidney-metabolic (CKM) syndrome stages 0–3 using NHANES 2005–2018 and UK Biobank cohorts. Across these CKM stages, diet pattern and micronutrient measures were tested using multivariable models to determine associations with subsequent MACE and death. The results are intended to clarify whether specific dietary exposures could be targeted for risk reduction in CKM-spectrum populations.

Hou Y, Yuan K, Xu Y et al. · Food science & nutrition · (2026) · View on PubMed ↗ · Free PDF ↗

PROMETHEUS clinical trial protocol: tailoring healthy ageing with lifestyle and nutraceuticals.

This paper describes the PROMETHEUS clinical trial protocol, an 8-week feasibility and exploratory study in 20 middle-aged-to-older participants testing a multimodal, tailored healthy-ageing intervention. The intervention combines sleep and dietary recommendations with nutraceutical supplementation (whey protein, creatine, fucoidan) and supervised exercise, aiming to target biological processes of ageing. If successful, the study will generate early evidence on feasibility and potential healthspan-relevant effects to support precision geromedicine approaches.

Kuerec AH, Guan L, Wang W et al. · GeroScience · (2026) · View on PubMed ↗ · Free PDF ↗

Moderate Intensity Resistance Training With Partial Range-of-Motion at Long Muscle Lengths Elicits Similar Hypertrophy and Architectural Adaptations as High Intensity Resistance Training Using Full Range-of-Motion.

This study randomized 45 subjects to compare moderate-intensity resistance training with partial range-of-motion at long muscle lengths versus high-intensity resistance training using full range-of-motion, focusing on chronic adaptations in muscle thickness and architecture. The abstract indicates that the moderate-intensity partial-ROM protocol produced similar hypertrophy and architectural adaptations to the high-intensity full-ROM protocol. Scientifically, this supports the idea that training at long muscle lengths can replicate key structural outcomes, potentially enabling more joint-friendly or time-efficient resistance training prescriptions.

McMahon G, Morse C, Burden A et al. · Journal of strength and conditioning research · (2026) · View on PubMed ↗

Appetite Suppression by GLP-1 Receptor Agonists: Role of Delayed Gastric Emptying.

This secondary analysis of a 16-week randomized, placebo-controlled liraglutide trial in adults with obesity examined how solid-food gastric emptying relates to appetite measures (satiation and energy intake) at baseline and end of treatment. Liraglutide-associated appetite suppression correlated with delayed gastric emptying, and patients with persistently delayed emptying showed different appetitive responses than those with normal emptying. These findings support a mechanistic link between GLP-1 receptor agonist effects on gastric motility and reduced energy intake, informing how to predict or optimize response to liraglutide in obesity.

Friedman MI, Harmsen WS, Camilleri M · Obesity (Silver Spring, Md.) · (2026) · View on PubMed ↗ · Free PDF ↗

Psychological stress drives aging-like hematopoietic stem cell dysfunction through a brain-gut-bone marrow axis.

The study investigated how psychological stress affects hematopoietic stem cell (HSC) function in relation to a brain–gut–bone marrow axis, focusing on neuronal activity in the medial prefrontal cortex (mPFC) and periaqueductal gray (PAG) and downstream gut metabolites. Chronic stress impaired HSC self-renewal and lymphoid differentiation into aging-like phenotypes, and chemogenetic activation of mPFC/PAG restored HSC function while stress reduced gut L. reuteri abundance and spermidine levels. These findings link stress-driven neuronal suppression to spermidine depletion and mitochondrial dysfunction, suggesting spermidine or microbiome/neuronal targets as potential interventions to prevent stress-associated HSC aging.

Tian X, Wu B, Yang K et al. · Cell stem cell · (2026) · View on PubMed ↗

Accelerometry-measured prolonged and interrupted sedentary behavior and cancer incidence and mortality: A cohort study of 91,292 UK Biobank participants.

This cohort study analyzed accelerometer-measured sedentary behavior patterns—specifically prolonged versus interrupted sedentary time—in 91,292 UK Biobank participants. Using a two-step random-forest classification and multivariable Cox models, it found differential associations of interrupted versus prolonged sedentary behavior with incident cancers and cancer mortality (including obesity- and type-2-diabetes–related cancers and multiple site-specific cancers). The findings refine sedentary behavior risk assessment beyond total sedentary time and support more specific behavioral targets for cancer prevention.

Zhou Z, Trost SG, Ryde GC et al. · PLoS medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Risk and Protective Factors for Suicide Mortality in Youths: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis synthesized evidence on risk and protective factors for suicide mortality in youths aged ≤24 years. It included case-control and cohort studies comparing youths who died by suicide with living general-population controls, searching MEDLINE, PsycINFO, Embase, and CINAHL through March 7, 2025. The clinical significance is that it provides an evidence-based, youth-specific map of factors associated with suicide mortality to guide prevention and risk stratification.

Geoffroy MC, Baker-Sullivan E, Nitu NJ et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Contraceptive Progestogens and Incident Meningioma.

This Danish nationwide nested case-control register study examined whether contraceptive progestogens are associated with incident meningioma in 3 million females aged 15–59 years. By matching meningioma cases to 10 controls on age, birthplace, and marital status and analyzing exposure over a 25-year period (2000–2024), it assessed differential meningioma risk across progestogen types used for contraception. The significance is improved quantification of contraceptive progestogen safety for meningioma risk, informing clinical counseling and prescribing decisions.

Hasselblad Lundstrøm N, Hjorslev Knudgaard M, Skaarup Pedersen M et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Early Access and Adherence to Physiotherapy in Children With Cerebral Palsy: Hospital-Based Study in Cameroon.

This hospital-based cross-sectional mixed retrospective/prospective study examined factors associated with early access and adherence to physiotherapy among children aged 3 to 60 months with cerebral palsy (CP) in Douala, Cameroon. Only 38.3% accessed physiotherapy early (before 5 months of age) and 38.3% achieved good adherence (completing ≥50% of prescribed sessions). Identifying barriers to timely initiation and sustained attendance is clinically significant for improving functional outcomes in pediatric CP where service access may be limited.

Enyama D, Moumeni IN, Fongang ES et al. · Pediatric physical therapy : the official publication of the Section on Pediatrics of the American Physical Therapy Association · (2026) · View on PubMed ↗ · Free PDF ↗

Adipokine dysregulation and oxidative stress in type 2 diabetes: Implications for neurodegeneration and neuroprotective eff ects of antidiabetic therapies.

This narrative review synthesized evidence on adipokine dysregulation and oxidative stress in type 2 diabetes and how these processes may contribute to neurodegeneration, including Alzheimer’s and Parkinson’s disease, and cognitive decline. It summarizes molecular pathways linking diabetic adipokine imbalance and oxidative stress to neuroinflammation and neurodegenerative mechanisms, and discusses potential neuroprotective effects of antidiabetic therapies. Clinically, the review frames adipokines and oxidative stress as actionable mechanistic links between metabolic disease and neurodegeneration, guiding future therapeutic strategies.

Kashmoola IO, Mohammad SH, Alsaaty MH · Neuropsychopharmacologia Hungarica : a Magyar Pszichofarmakologiai Egyesulet lapja = official journal of the Hungarian Association of Psychopharmacology · (2026) · View on PubMed ↗

Clinical and mechanistic effects of GLP-1 receptor agonists in hidradenitis suppurativa and comorbidities.

This narrative review evaluated clinical and mechanistic effects of GLP-1 receptor agonists (GLP-1RAs) in hidradenitis suppurativa (HS) and related comorbidities by synthesizing evidence from 12 cohorts and 4 case reports. Across included studies, GLP-1RA treatment was associated with improvements in HS clinical and patient-reported outcomes alongside reductions in BMI and disease activity. The findings suggest GLP-1RAs may benefit HS patients—particularly those with obesity and metabolic comorbidities—through mechanisms that connect metabolic regulation to inflammation.

Brogaard E, Nielsen VW, Pedersen NH et al. · Science progress · (2026) · View on PubMed ↗ · Free PDF ↗

The impact of the six pillars of lifestyle medicine on the biology of skin aging.

This narrative review examined how the six pillars of lifestyle medicine—nutrition, physical activity, stress regulation, sleep, avoidance of toxic exposures, and social connection—affect the biology of skin aging. It links modifiable lifestyle factors to key skin-aging pathways including mitochondrial dysfunction, oxidative stress, chronic inflammation, cellular senescence, and extracellular matrix remodeling. By connecting behavior to molecular mechanisms, the review supports lifestyle-based strategies as biologically grounded interventions to slow or mitigate skin aging.

Piquero-Casals J, Cruz AR, Ponti-Concetti L et al. · Frontiers in aging · (2026) · View on PubMed ↗ · Free PDF ↗

Joint association of the frailty index and phenotypic age with all-cause and cause-specific mortality: A prospective cohort study.

The prospective NHANES-based cohort study assessed whether frailty index (FI) and phenotypic age (PhenoAge) jointly predict all-cause and cause-specific mortality in adults, using data from 2003–2010 with follow-up through 2019. FI and PhenoAge were evaluated with Cox proportional hazards and competing risk models to determine independent and interactive associations with death risk. Demonstrating joint predictive value would improve risk stratification by capturing biological aging and frailty beyond chronological age.

Shao Z, Zhao Y, Yang H et al. · Journal of translational internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗

---

---

Generated automatically on July 04, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.