PubMed Trending Research Digest — June 04, 2026

Automated digest · 97 articles · 15 research areas · June 04, 2026

Overview

Across this week’s papers, a dominant thread is the move from single-mechanism thinking toward network-level, translational strategies—linking immune signaling, metabolism, and tissue microenvironments to disease progression and treatment response. In oncology, multiple studies emphasize pathway rationales and resistance mechanisms (e.g., MEK/autophagy–STING crosstalk in cholangiocarcinoma, S1P resensitization in NRAS-mutant FLT3-ITD AML, enhancer remodeling and mevalonate pathway activation in KRAS inhibitor resistance, and nucleophagy components shaping PARP inhibitor adaptation). In parallel, immunotherapy-focused work (including adoptive cell therapy correlates and AD immunotherapy bibliometrics) underscores the importance of patient- and tumor-specific immune states for predicting benefit.

A second major theme is biomarkers and precision stratification—spanning neurodegeneration, infectious disease, and clinical genomics. Gut microbiome composition/metabolites and diet-driven microbiome remodeling are repeatedly positioned as both biomarkers and therapeutic targets for neurodegenerative disease and beyond. For neurodegeneration, plasma markers such as p-tau217 and serum neurofilament proteins (including sNfH) are advanced for diagnosis and risk prediction, while imaging and MRI-based approaches improve differential diagnosis (e.g., PSP vs parkinsonisms). In hematology and neurology, updated consensus frameworks (HLA matching in HCT; gene-specific variant interpretation for SCN-related epilepsies; and international benchmarks for pediatric epilepsy surgery pathways) aim to standardize decision-making and reduce variability.

Finally, several studies highlight how lifestyle and host physiology can be mechanistically leveraged—through circadian-aligned feeding, resistance training, and exercise-driven modulation of neuroinflammation, as well as targeted manipulation of cell-death/inflammatory programs (ferroptosis, NETosis, necroptosis-associated pathways) and metabolic vulnerabilities (including refined mechanisms of metformin/biguanide toxicity). Together, these findings reinforce a broad shift toward actionable biology: identifying druggable nodes (immune axes, cell-death pathways, metabolic switches) and pairing them with measurable biomarkers and stratified clinical strategies to improve outcomes.

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Gut microbiome & gut–brain axis biomarkers/therapies

15-strain live biotherapeutic product or same donor fecal microbiota transplant for recurrent Clostridioides difficile infection: a randomized phase 1b trial.

This randomized phase 1b trial compared a 15-strain live biotherapeutic product (LBP) versus fecal microbiota transplant (FMT) using the same donor-derived bacterial strains in patients with recurrent Clostridioides difficile infection (rCDI). The study reported that the defined 15-strain LBP could be manufactured using an accessible human-grade platform and directly compared against the same donor FMT composition to evaluate safety and clinical performance. This work is significant because it provides a scalable, composition-defined alternative to FMT for rCDI while supporting regulatory/manufacturing pathways for future LBP development.

Bethlehem L, Bartu L, Marke G et al. · Nature medicine · (2026) · View on PubMed ↗

TadA-mediated A-to-I mRNA editing rewires redox metabolism to promote dominance of epidemic Klebsiella pneumoniae clones.

This study mapped adenosine-to-inosine (A-to-I) mRNA editing landscapes in clinically dominant carbapenem-resistant Klebsiella pneumoniae (CRKP) epidemic clones and identified key editing targets. It found that dominant lineages have a constrained, clone-specific RNA editing program and highlighted PncR (an AraC/XylS-family transcription factor) and DcuR as prominent A-to-I editing targets. These results suggest that RNA editing—rather than only fixed DNA mutations—can rewire bacterial regulatory networks and redox metabolism to promote the success of epidemic CRKP clones.

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

Ketogenic Diets and Low Carb Diets: The Effects on the Intestinal Microbiota. A Narrative Review.

This narrative review studied how ketogenic diets (KDs) and low-carbohydrate diets (LCDs) affect the human gut microbiota across adult populations (18–74 years; healthy adults including normal-weight, overweight, and obese individuals). It found that carbohydrate restriction is associated with distinct taxonomic shifts in gut microbial composition across the included 10 studies (n=346), suggesting diet-driven microbiome remodeling. The review is significant because it links dietary macronutrient composition to microbiome changes that may influence host metabolism and health outcomes.

Bertuccioli A, Sisti D, Palazzi CM et al. · Nutrition reviews · (2026) · View on PubMed ↗

The gut-brain axis in Alzheimer’s and Parkinson’s diseases: a systematic review of microbiota-derived biomarkers and novel therapeutic approaches.

This systematic review evaluated clinical and preclinical evidence (2010–2025) on gut microbiota composition and microbiota-derived metabolites as biomarkers and therapeutic targets in Alzheimer’s disease (AD) and Parkinson’s disease (PD). It found that gut-brain axis alterations and microbiome-derived metabolites are repeatedly linked to disease onset/progression and may support diagnostic biomarker development and novel therapeutic approaches. These findings support further translational work to validate microbiota-derived biomarkers and to test microbiome-targeted interventions for AD and PD.

Singh VK, Gupta P, Jain SK et al. · Journal of clinical and experimental neuropsychology · (2026) · View on PubMed ↗

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Immunology of vaccines & immune activation biomarkers

Heterogeneity of baseline immune activation and SARS-CoV-2 vaccine responses in people with HIV: a multicenter prospective study.

This multicenter prospective study measured baseline plasma levels of 20 cytokines, chemokines, and soluble endothelial markers in 159 antiretroviral therapy (ART)-treated people with HIV (PWH) across two immunovirological control profiles and 56 HIV-negative controls to assess heterogeneity in SARS-CoV-2 vaccine responses. Baseline immune activation/inflammation differed by HIV immunovirological control status and was associated with variability in vaccine-induced immunity. The results suggest that stratifying PWH by baseline immune activation could improve prediction of vaccine responsiveness and guide tailored immunization strategies.

Moussaou ME, Ladang A, Maes N et al. · AIDS (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Epigenetic regulation & chromatin acetylation

The roles of the acetyltransferase domains of the KAT6A and KAT6B in vivo.

This in vivo study investigated whether the acetyltransferase (KAT) domains of the histone lysine acetyltransferases KAT6A (MOZ) and KAT6B (QKF/MORF) are required for their developmental functions. Loss of KAT6A acetyltransferase activity did not phenocopy loss of the KAT6A protein, indicating that KAT6A’s developmental roles are not solely dependent on its acetyltransferase activity. These findings refine mechanistic understanding of KAT6A/KAT6B redundancy and inform how acetyltransferase function versus protein-specific roles contribute to developmental phenotypes.

Thomas T, Malelang S, Yang Y et al. · Development (Cambridge, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Endocrine/metabolic drug effects & adverse events (GLP-1/GIP, etc.)

Anti-asthma drug montelukast induces autistic behaviors via disrupting neuronal retinoic acid signaling.

This preclinical study tested whether montelukast (MTK), a cysteinyl leukotriene receptor antagonist, can induce autism-like behaviors by disrupting neuronal retinoic acid (RA) signaling. Prenatal or early postnatal MTK exposure in wild-type rats altered synaptic plasticity in primary rat prefrontal cortex neurons, disrupted neuronal RA signaling, and produced autistic-like behaviors that were partially alleviated by intervention targeting the RA pathway. The findings are significant because they raise a mechanistic safety concern for MTK exposure during development and implicate RA signaling disruption in ASD-like phenotypes.

Hao ZJ, Wu QH, Li YL et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Glucagon-like peptide 1 receptor agonist use and risk of arthroplasty for knee osteoarthritis: retrospective database analysis.

This retrospective database analysis assessed whether glucagon-like peptide 1 receptor agonists (GLP-1 RAs) reduce progression to total knee arthroplasty (TKA) in adults with knee osteoarthritis (OA) using the TriNetX Global Research Network. Patients were stratified by GLP-1 RA exposure (including semaglutide and tirzepatide) and compared for TKA risk over follow-up. If GLP-1 RA exposure lowers TKA risk, it would support a disease-modifying or progression-slowing role for these agents in knee OA beyond symptom relief.

Carter V, Desverreaux E, Amin I et al. · Regional anesthesia and pain medicine · (2026) · View on PubMed ↗

Beyond weight loss: How metabolism in human adipocytes is shaped by GLP-1R agonists and dual GIPR/GLP-1R agonists.

This review summarized how GLP-1 receptor agonists and dual GIPR/GLP-1R agonists (including tirzepatide) shape metabolism in human adipocytes. It focused on mechanistic effects of these incretin-based drugs on adipocyte metabolic pathways relevant to obesity and related comorbidities. The significance is a clearer biological rationale for the metabolic benefits of GLP-1RAs and tirzepatide that extend beyond weight loss.

Curto R, Giglione C, Cannarella R et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

15-PGDH inhibition promotes muscle repair and strength recovery during GLP-1 receptor agonist-induced weight loss.

This study tested whether inhibiting 15-hydroxyprostaglandin dehydrogenase (15-PGDH) can protect skeletal muscle during GLP-1 receptor agonist–induced weight loss, using semaglutide-treated high-fat diet–induced obese mice. It found that 15-PGDH inhibition promoted muscle repair and strength recovery, counteracting semaglutide-associated muscle mass loss while preserving contractile function. The work supports 15-PGDH inhibition as a potential adjunct therapy to mitigate muscle adverse effects during GLP-1 receptor agonist treatment.

Nalbandian M, Lone J, Le Moal E et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

GLP-1 Agonists Are Associated With a Significant Reduction in Breast Cancer Incidence in Women.

This retrospective cohort study assessed whether glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are associated with breast cancer incidence reduction in women aged 45–80 with BMI ≥25 using electronic health records from 2022–2025. The key finding was a significant reduction in breast cancer incidence among GLP-1 RA users compared with non-users (details truncated in the abstract). This supports a potential protective association between GLP-1 RA exposure and breast cancer risk, warranting prospective validation and mechanistic investigation.

McDonald ES, Gillis LB, Gabriel P et al. · JCO oncology practice · (2026) · View on PubMed ↗ · Free PDF ↗

Pharmacovigilance Assessment of Thrombotic Adverse Events Linked to GLP-1 Receptor Agonists: Analysis of FAERS Reports from 2020-2025.

This pharmacovigilance study analyzed FDA Adverse Event Reporting System (FAERS) reports from 2020–2025 to assess reporting of thrombotic adverse events associated with GLP-1 receptor agonists (GLP-1 RAs). The key finding was based on disproportionality testing using reporting odds ratios and time-to-onset analyses, with comparisons to orlistat and SGLT2 inhibitors (specific results truncated in the abstract). Scientifically, it helps quantify potential safety signals for thrombosis with GLP-1 RAs and can guide clinicians and regulators toward targeted risk evaluation.

Mansory EM, Radhwi OO · Current drug safety · (2026) · View on PubMed ↗

Hypercalcemia Induced by Tirzepatide and Calcium Supplementation: A Case Report.

This case report described a 70-year-old woman who developed hypercalcemia after starting tirzepatide (a GLP-1R/GIPR agonist) while taking exogenous calcium supplements for osteoporosis. The clinical course supports tirzepatide as a potential contributor to hypercalcemia in the setting of calcium supplementation. Clinically, it highlights the need to monitor calcium levels and consider risk factors when prescribing tirzepatide, especially in patients using calcium supplements.

Nguyen E, Kawamura M, Munoz I et al. · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

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Depression & bipolar disorder pharmacotherapy (next-gen approaches)

Next-Generation Pharmacotherapy for Depressive Disorders: From Novel Compounds to Optimized Use of Available Drugs.

This narrative review synthesized evidence on next-generation pharmacotherapy for depressive disorders, with emphasis on treatment-resistant depression (TRD) and bipolar depression where conventional monoaminergic antidepressants often have delayed onset, incomplete response, relapse, and tolerability limitations. It concluded that mechanism-informed development and optimized use of existing drugs can address unmet needs by targeting non-monoaminergic pathways and improving practical outcomes. Scientifically and clinically, the review supports continued drug discovery and rational treatment strategies to improve remission rates and tolerability in difficult-to-treat depression subtypes.

Bu F, Qin L, Lou Z et al. · Drug design, development and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

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Embryogenesis & post-transcriptional RNA regulation

A 3’UTR-derived small RNA modulates the life cycle of the cholera toxin-encoding filamentous phage, CTXϕ.

This study investigated a 3’UTR-derived small RNA that modulates the life cycle of the cholera toxin-encoding filamentous phage CTXϕ in Vibrio cholerae. The authors reported that the small RNA regulates CTXϕ biology in a way that affects the phage’s ability to control its toxin-encoding program (ctxAB) during the phage life cycle. This provides mechanistic insight into how noncoding RNAs can tune cholera toxin phage propagation and horizontal gene transfer.

Lippegaus A, Haycocks JRJ, O’Driscoll E et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

FUS modulates R-loops by functionally interacting with RNase H1.

This study investigated how the RNA-binding protein FUS (mutated in amyotrophic lateral sclerosis and cancer) modulates R-loops by functionally interacting with RNase H1 in human cells. It found that FUS influences R-loop homeostasis through RNase H1–related regulation, with dysregulated R-loop accumulation contributing to DNA damage and genomic instability. The work is significant because it connects an ALS/cancer-associated gene (FUS) to a specific genome-protective RNA–DNA hybrid processing pathway (RNase H1/R-loop control).

Dey A, Das R, Uppal S · Human cell · (2026) · View on PubMed ↗

The SPN-4 Rbfox RNA-binding protein selects maternal mRNAs for CCR4-NOT-dependent clearance in early Caenorhabditis elegans embryos.

This study in early Caenorhabditis elegans embryos examined how the SPN-4 Rbfox RNA-binding protein selects maternal mRNAs for clearance via the CCR4-NOT deadenylase complex during the maternal-to-zygotic transition. Using biochemical identification and single-molecule fluorescence in situ hybridization, the authors showed that SPN-4-associated maternal mRNAs are enriched for early-decaying transcripts and that many fail to be eliminated without SPN-4. These results define a specificity mechanism (SPN-4) that directs CCR4-NOT-dependent maternal mRNA clearance, advancing understanding of post-transcriptional control in embryogenesis.

Spike CA, Parker DM, Tsukamoto T et al. · Development (Cambridge, England) · (2026) · View on PubMed ↗

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Targeted oncology: RAS/MEK, KRAS resistance, and pathway combinations

Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with NRAS mutations to FLT3 inhibitors.

The study tested whether sphingosine-1-phosphate receptor (S1PR) modulators can resensitize NRAS-mutated FLT3-ITD acute myeloid leukemia (AML) cells to FLT3 inhibitors, using NRAS-mutated FLT3-ITD AML cell lines, patient blasts, and an orthotopic in vivo model. Co-targeting FLT3 and S1P signaling improved FLT3 inhibitor sensitivity, assessed by immunoblotting, cytotoxicity, apoptosis, and colony formation, and enhanced therapeutic response in vivo. This supports a combination strategy targeting S1P receptor signaling to overcome common NRAS-driven resistance to FLT3 inhibitors in AML.

Chatterjee A, Mustafa Ali MK, Bailey CM et al. · Leukemia · (2026) · View on PubMed ↗

Mevalonate pathway rewiring driven by enhancer remodelling confers resistance to KRAS inhibitors in colorectal cancer.

This study investigated mechanisms of resistance to KRAS inhibitors in KRAS-mutant colorectal cancers by analyzing enhancer remodeling and its effects on cholesterol biosynthesis via the mevalonate (MVA) pathway. It found that KRAS inhibitor–resistant colorectal cancers show ERK reactivation and that enhancer remodeling activates the MVA pathway, enabling KRAS trafficking to the membrane and sustaining MAPK signaling despite KRAS inhibition. The work is significant because it supports combining KRAS pathway inhibitors with statins (MVA pathway blockade) as a strategy to overcome or prevent KRAS inhibitor resistance.

Guo Y, Zhong Y, Hu P et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

USP2 is an androgen-repressed survival factor that stabilises oncoproteins to facilitate therapy resistance in prostate cancer.

This study investigated ubiquitin-specific peptidase 2 (USP2) as an androgen-repressed survival factor in prostate cancer cells and castration-resistant prostate tumors undergoing androgen receptor (AR)-targeted therapies and/or docetaxel. USP2 was induced by AR-targeted therapies, overexpression increased glycolysis and neuroendocrine features, and USP2 stabilized oncoproteins to promote resistance to docetaxel. These findings identify USP2 as a therapy-resistance mediator and a potential target to overcome AR-therapy and chemotherapy resistance in advanced prostate cancer.

Fang DM, Shrestha RK, German B et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Phase 1b trial of Bavdegalutamide (ARV-110) in combination with Abiraterone for metastatic prostate cancer.

This phase 1b trial studied the oral PROTAC androgen receptor (AR) degrader bavdegalutamide (ARV-110) combined with abiraterone in men with metastatic prostate cancer (mPC) who had PSA progression on abiraterone. The study evaluated safety/tolerability (including dose-limiting toxicities) and pharmacokinetics, with the key reported outcome being the regimen’s ability to be administered in this resistant population while characterizing exposure and PSA control (details truncated in the abstract). If tolerability and pharmacodynamic activity are confirmed, this combination could provide a new strategy to overcome resistance to androgen receptor pathway inhibitors in mPC.

Smoragiewicz M, Bernard-Tessier A, Linch M et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗ · Free PDF ↗

Ziftomenib with venetoclax and azacitidine in relapsed/refractory NPM1-mutated acute myeloid leukemia.

This report analyzed adults with relapsed/refractory (R/R) NPM1-mutated acute myeloid leukemia (AML) treated in the KOMET-007 phase 1 trial with the oral menin inhibitor ziftomenib plus venetoclax and azacitidine. The key finding was the trial’s observed clinical activity and tolerability of the combination across phase 1a dose levels and a phase 1b expansion cohort (specific response rates truncated in the abstract). If efficacy is confirmed, ziftomenib-based triplet therapy could improve outcomes for NPM1-mutated AML patients who relapse after standard treatments.

Wang ES, Erba HP, Zeidan AM et al. · Blood · (2026) · View on PubMed ↗

Combined MEK1/2 and Autophagy Inhibition Suppresses Tumor Growth via STING-Mediated Type I Interferon Response in iCCA.

This study investigated how combined MEK1/2 inhibition and autophagy inhibition affects intrahepatic cholangiocarcinoma (iCCA) tumor growth, focusing on STING-mediated type I interferon signaling. MEK inhibition triggered protective autophagy that limited cGAS–STING–TBK1 activation, whereas blocking autophagy restored/strengthened the STING-driven type I interferon response and suppressed tumor growth. The work supports a rational combination strategy (MEK inhibition plus autophagy blockade) to overcome MEK inhibitor resistance in iCCA via innate immune activation.

Sun C, Gao Z, Dong E et al. · Cancer science · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical oncology trials & treatment outcomes (including immunotherapy/ADCs)

Obexelimab for the Treatment of IgG4-Related Disease.

This phase 3 randomized, double-blind, placebo-controlled trial studied obexelimab, a bifunctional monoclonal antibody that co-engages CD19 and FcγRIIb to inhibit B-cell activity without depletion, in patients with active IgG4-related disease. Obexelimab given subcutaneously at 250 mg once weekly for 52 weeks with standardized glucocorticoid tapering was evaluated for efficacy and safety versus placebo. If effective, this would provide a glucocorticoid-sparing, relapse-reducing immunotherapy option for IgG4-related disease with a distinct mechanism from B-cell depletion.

Della-Torre E, Baker MC, Zhang W et al. · The New England journal of medicine · (2026) · 1 citations · View on PubMed ↗

Dietary patterns, metabolic pathways and metainflammation in hidradenitis suppurativa: a systematic review.

This systematic review evaluated evidence on dietary patterns, nutritional interventions, and micronutrient status in hidradenitis suppurativa (HS) and how these factors may influence metainflammation and immunometabolic pathways. The authors conclude that HS behaves as a systemic immunometabolic disease and that diet could modulate HS activity through metabolic and inflammatory mechanisms linked to comorbid obesity, insulin resistance, and metabolic syndrome. Clinically, the review supports further dietary research to identify actionable nutritional strategies that may improve HS disease control.

Celik E, Bechara FG, Stockfleth E et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial, temporal, and molecular heterogeneity of ADC targets in high-grade serous ovarian carcinoma.

This study investigated spatial, temporal, and molecular heterogeneity of antibody-drug conjugate (ADC) targets in high-grade serous ovarian carcinoma (HGSOC) using two tissue microarray cohorts. Across 100 genomically profiled cases (1565 cores) and 64 matched cases with paired adnexal, locally advanced, and recurrent samples (2395 cores), the authors analyzed how ADC target expression varied by sampling site and molecular features and related these patterns to survival. The results are intended to improve patient selection and dosing strategies for ADC therapy by accounting for intratumoral and disease-stage target heterogeneity.

Li X, Janik T, Möbs M et al. · British journal of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

LGALS1-CD276 Paracrine axis between tumor and endothelial cells promotes tumor angiogenesis and progression in bladder cancer.

The authors investigated the tumor–endothelial paracrine mechanism in bladder cancer by identifying binding partners of CD276 (B7-H3) and testing the functional role of the LGALS1–CD276 axis. Using a high-throughput human proteome microarray, they found that secreted galectin-1 (LGALS1) binds CD276 with high affinity and that this LGALS1–CD276 signaling in endothelial cells promotes tumor angiogenesis and progression. This defines a new ligand–receptor axis that could be exploited to therapeutically disrupt bladder cancer vascularization.

Liu Z, Yao Z, Hou Y et al. · Cell death and differentiation · (2026) · View on PubMed ↗

Hallmarks and correlates of effective adoptive cell immunotherapy for cancer.

This Nature Reviews Immunology article synthesized evidence on the immunogenomic and systems-level hallmarks that correlate with effective adoptive cell immunotherapy (ACT) across cancers. It highlights that neoantigen-specific T cells delivered as tumor-infiltrating lymphocytes (TILs) or TCR-engineered T cells (TCR-T) can drive tumor regression in multiple metastatic solid tumors, and it summarizes correlates from immunogenomics and systems immunology. The review provides a framework for predicting and improving ACT responsiveness in patients with otherwise resistant solid epithelial cancers.

Krishna S, Robbins PF, Lowery FJ et al. · Nature reviews. Immunology · (2026) · View on PubMed ↗

Integrative analyses elucidate transcriptional regulatory functions of risk alleles for metabolic liver disease.

The study integrated genome-wide association study (GWAS) risk loci with chromatin accessibility mapping in human MASLD liver nuclei and used massively parallel reporter assays to test regulatory variant function. It found that MASLD risk variants are enriched in cell-type-specific regulatory elements bound by lineage-determining transcription factors, and reporter assays identified hundreds of differential activity variants (DAVs) that perturb liver transcriptional regulatory networks in a cell-type- and stimulus-dependent manner. These integrative analyses clarify how noncoding risk alleles regulate gene networks underlying metabolic liver disease and steatotic liver pathology.

Zhu B, He N, Xiao Y et al. · Nature genetics · (2026) · View on PubMed ↗

Pharmacological treatment of schizophrenia: Japanese Expert Consensus 2025.

This Japanese Expert Consensus 2025 surveyed 154 board-certified psychiatrists to update practical schizophrenia pharmacotherapy guidance across 21 clinical scenarios using a 9-point Likert rating system. The consensus emphasized symptom-dependent selection among first-line antipsychotics, including risperidone, brexpiprazole, olanzapine, and paliperidone, reflecting current routine practice needs. Clinically, it standardizes decision-making for real-world prescribing in Japan and helps align treatment choices with specific symptom profiles and situational considerations.

Takekita Y, Tani H, Kawamata Y et al. · Schizophrenia (Heidelberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Recombinant Bombali ebolavirus in cynomolgus macaques as a survival model of Ebola virus disease.

The study evaluated whether recombinant Bombali orthoebolavirus (rBOMV) can serve as a survival model of Ebola virus disease by challenging cynomolgus macaques. Infected macaques developed hallmark Ebola-like pathology including vascular leak, lymphopenia, neutrophilia, elevated inflammatory markers, and detectable rBOMV across multiple target tissues at peak viremia. This is significant because it provides a practical non-human primate model for Bombali ebolavirus disease biology and for testing countermeasures.

Turcinovic J, Fenton KA, Agans KN et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Atopic dermatitis Yardstick: a new era of topical and systemic treatments.

This article is an evidence-based clinical “Yardstick” update reviewing current topical and systemic treatments for atopic dermatitis (AD), including newly added therapies. It highlights medications such as roflumilast cream, tapinarof cream, lebrikizumab, and nemolizumab and provides updated practical guidance for clinicians, including patient vignettes. The significance is improved, up-to-date treatment selection and implementation for AD in routine practice.

De Benedetto A, Boguniewicz M, Fonacier L et al. · Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · (2026) · View on PubMed ↗

An International, Multi-Specialty Consensus Document on the Optimal Management of Patients with Internal Carotid Artery Occlusion.

This international multi-specialty consensus document synthesized evidence on the optimal management of patients with internal carotid artery occlusion (ICAO), an advanced stage of atherosclerotic carotid disease. It collated literature from 1980–2025 (after exclusions) to address associations with vascular risk factors and implications for patient care. The significance is standardized, evidence-informed guidance for clinicians managing ICAO across vascular risk profiles and comorbid atherosclerotic disease.

Paraskevas KI, Sultan S, Podlasek A et al. · Journal of vascular surgery · (2026) · View on PubMed ↗

Final outcomes of the SOFT and TEXT phase III trials in premenopausal hormone receptor-positive early breast cancer.

The SOFT and TEXT phase III trials studied adjuvant endocrine strategies in premenopausal women with hormone receptor-positive early breast cancer (SOFT n=3047; TEXT n=2660), comparing tamoxifen (T) alone versus T plus ovarian function suppression (OFS) versus exemestane (E) plus OFS. At 15 years, adding OFS to tamoxifen and using exemestane+OFS further reduced breast cancer recurrence, with the combined analysis showing a significant reduction in distant recurrence for E+OFS versus T+OFS. These long-term results support aromatase inhibition with OFS as a more effective standard for higher-risk premenopausal patients than tamoxifen+OFS.

Francis PA, Pagani O, Fleming GF et al. · Annals of oncology : official journal of the European Society for Medical Oncology · (2026) · View on PubMed ↗

Global burden of enteric infectious diseases, diarrhoeal diseases, and corresponding aetiologies, 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023.

This Global Burden of Disease Study 2023 systematic analysis quantified global incidence, mortality, and etiologies of enteric infectious diseases and diarrhoeal diseases from 1990–2023, focusing on children under 5 years and progress toward the GAPPD pneumonia-and-diarrhoea mortality target. The study reports updated epidemiological estimates and assesses whether recent trends indicate sustained progress or emerging setbacks in enteric disease control. The findings provide evidence to guide where prevention and treatment investments should be intensified or redirected to reduce diarrhoea-related deaths.

The Lancet. Infectious diseases · (2026) · View on PubMed ↗

Real-world emergence of nirsevimab resistance in breakthrough infections with respiratory syncytial virus-B: a multicentre observational study in France.

A multicentre observational study in France examined real-world nirsevimab breakthrough infections in RSV-B and characterized viral escape using genotypic and phenotypic assays during the 2024–2025 RSV season. The key finding was evidence of nirsevimab resistance/escape emerging in RSV-B breakthrough cases at scale, indicating that resistant variants can arise under antibody pressure. This matters for RSV prevention policy because it informs surveillance and potential need for updated or combination strategies if resistance becomes more prevalent.

Fourati S, Reslan A, Bourret J et al. · The Lancet. Microbe · (2026) · View on PubMed ↗ · Free PDF ↗

Outcomes of Y90-radioembolization as downstaging to liver transplantation in patients with hepatocellular carcinoma and tumoral portal vein thrombosis.

This multicenter Italian cohort study assessed outcomes after Y90 transarterial radioembolization (TARE) used as downstaging therapy in patients with hepatocellular carcinoma (HCC) and tumoral portal vein thrombosis (PVTT) who subsequently underwent liver transplantation. The key finding was that patients who achieved successful downstaging with sustained radiological response for at least 6 months had post-LT oncologic and survival outcomes that supported feasibility of LT after TARE downstaging. Clinically, it provides evidence that PVTT is not an absolute contraindication when durable response to Y90 enables transplantation.

Sposito C, Berardi G, Viganò M et al. · Hepatology (Baltimore, Md.) · (2026) · View on PubMed ↗

Global Consensus on Keratoconus and Ectatic Diseases-Edition 2.

This article used a Delphi consensus process (4 questionnaire rounds plus a face-to-face meeting) with 128 ophthalmologists from 12 international societies to update global guidance on keratoconus and ectatic corneal diseases. The key output was an expert consensus on definitions, diagnosis, staging, clinical management, and surgical treatment, incorporating advances in new technologies. Clinically, it standardizes care pathways worldwide and helps harmonize decision-making for patients with keratoconus and related ectatic disorders.

Gomes JAP, Hafezi F, Ambrósio R et al. · Cornea · (2026) · View on PubMed ↗

An orally active dual CBP/p300 degrader targets core dependencies of multiple myeloma.

This work studied an orally active targeted protein degradation strategy against the enhancer acetyltransferases CBP/p300 in multiple myeloma, comparing degradation to bromodomain/catalytic inhibition across many cell lines. The authors demonstrated that CBP/p300 degradation—via an optimized chemical linker approach building on dCBP-1—produced pronounced selective antiproliferative effects in multiple myeloma models. This supports CBP/p300 degraders as a more complete therapeutic modality than inhibition because degradation disrupts all functional domains simultaneously.

Tiwari PK, Ku B, Harrison DA et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Dermatologic Adverse Events Associated with T-Cell Engager Therapy.

This article reviewed dermatologic adverse events associated with T-cell engager cancer therapies, emphasizing bispecific T-cell engagers and the immune-mobilizing monoclonal T-cell receptor tebentafusp. It found that tebentafusp and talquetamab show the highest rates of clinically notable skin toxicity, with tebentafusp commonly causing diffuse erythematous, often photodistributed eruptions consistent with on-target off-tumor effects. The findings are clinically important for anticipating, recognizing, and managing cutaneous toxicities during T-cell engager treatment.

Patil MK, Wang B, LeBoeuf NR et al. · American journal of clinical dermatology · (2026) · View on PubMed ↗

Impact of appropriate antimicrobial therapy on patient outcomes and antimicrobial use: a sub analysis of the DIANA Study Dataset.

This predefined sub-analysis of the DIANA study dataset studied how appropriate empiric antimicrobial therapy influences outcomes and antimicrobial exposure in adult ICU patients with suspected or confirmed bacterial infection. It found that the prevalence of appropriate empiric therapy and its association with patient outcomes and antibiotic exposure could be quantified in a large international cohort restricted to microbiologically confirmed infections. The significance lies in refining evidence on when empiric antibiotic appropriateness improves ICU outcomes and how it affects antimicrobial use patterns.

Cidade JP, Póvoa P, Depuydt P et al. · Intensive care medicine · (2026) · View on PubMed ↗

CEBPG-Mediated Palmitic Acid Adaptation of Cancer-Associated Fibroblasts Drives Metastasis of Oral Squamous Cell Carcinoma.

This work investigated how palmitic acid (PA) reprograms cancer-associated fibroblasts (CAFs) via the fatty-acid transporter CD36 to drive metastasis of oral squamous cell carcinoma (OSCC), using in vitro 2D/3D/organoid co-culture and orthotopic in vivo models. PA potently activated myofibroblastic CAF phenotypes and promoted lymph node metastasis in OSCC–CAF orthotopic tumors, and this pro-metastatic effect was abolished by CD36 knockdown in CAFs. The findings identify a CD36-dependent PA–CAF axis as a mechanistic driver of OSCC metastasis and a potential therapeutic target in the tumor microenvironment.

Duan Y, Li Y, Wu Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Structure-Guided Optimization of Novel Inhibitors of Plasmodium Lysyl-tRNA Synthetase with Multistage Activity against Malaria Parasites.

This study used structure-guided medicinal chemistry to optimize inhibitors of Plasmodium lysyl-tRNA synthetase (KRS), starting from a fused dihydropyrrolidino-pyrimidine hit identified in the Global Health Chemical Diversity Library (GHCDL). Lead optimization produced a potent, highly selective basic KRS inhibitor (compound 30) with extended half-life that enabled a single-dose cure in the oral efficacy malaria NOD-scid-IL2Rγnull (SCID) mouse model. Scientifically and clinically, this provides a rationally designed antimalarial candidate with strong selectivity and dosing advantages, supporting further development toward single-dose regimens.

Forte B, Bellany F, Campbell PS et al. · Journal of medicinal chemistry · (2026) · View on PubMed ↗ · Free PDF ↗

Selinexor Plus Ruxolitinib in JAK Inhibitor-Naïve Myelofibrosis: Phase 3 SENTRY Trial.

This double-blind phase 3 SENTRY trial evaluated selinexor (an exportin 1/XPO1 inhibitor) plus ruxolitinib versus placebo plus ruxolitinib in JAK inhibitor–naïve myelofibrosis patients. The key finding was that the combination’s efficacy was assessed at Week 24 using co-primary endpoints of spleen volume reduction ≥35% (SVR35) and absolute mean change in total symptom score excluding fatigue (full results truncated in the abstract). If the combination outperforms ruxolitinib alone, it could improve both splenic and symptom outcomes while addressing clonal burden limitations.

Bose P, Ali H, Al-Ali HK et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Immunotherapeutic Innovations in Alzheimer’s Disease: A Bibliometric Landscape of Global Research Trends and Evolution.

This bibliometric study mapped global immunotherapy research for Alzheimer’s disease (AD) by analyzing 5,585 publications and identifying trends in antibody therapies and immune-modulation mechanisms. It found that the field has rapidly expanded with clear research “hotspots” around targeting amyloid-β and related immune pathways. These findings help prioritize emerging therapeutic directions and collaboration opportunities for future AD immunotherapy development.

Sun N, Liu Q, Wu P et al. · Current neuropharmacology · (2026) · View on PubMed ↗

Denosumab versus bisphosphonates for the management of bone metastases originating from breast cancer: a systematic review and meta-analysis.

This systematic review and meta-analysis compared denosumab with bisphosphonates for bone metastases from breast cancer, focusing on skeletal-related events (SREs) and adverse events. Across five publications (three randomized trials and one retrospective cohort), it evaluated relative efficacy and safety outcomes including renal, metabolic, hematologic, musculoskeletal, gastrointestinal, and infectious adverse events. The results aim to guide treatment selection by clarifying whether denosumab provides superior SRE control or different toxicity profiles versus bisphosphonates.

Boutros M, Awad G, Saad JP et al. · Future oncology (London, England) · (2026) · View on PubMed ↗

Efficacy and Safety of Newer Antibiotics Versus Generic Antibiotics for Hospital-Acquired and Ventilator-Associated Bacterial Pneumonia: A Systematic Review and Meta-analysis of Randomized Controlled Trials.

This systematic review and meta-analysis evaluated randomized controlled trials comparing newer antibiotics versus generic antibiotics for hospital-acquired bacterial pneumonia (HABP) and ventilator-associated bacterial pneumonia (VABP). It searched multiple databases for RCTs published between 2013 and 2025 and focused on efficacy and safety outcomes, particularly in settings involving multidrug-resistant organisms. The analysis is intended to clarify whether newer agents improve clinical outcomes or introduce different risks compared with generics in HABP/VABP management.

Nguyen ATK, Paterson DL, Mo Y et al. · Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · (2026) · View on PubMed ↗

Daraxonrasib Doubles OS for PDAC in Phase III Trial.

This report summarized results from a phase III trial in metastatic pancreatic ductal adenocarcinoma (PDAC) comparing the pan-RAS inhibitor daraxonrasib with chemotherapy as second-line treatment. Daraxonrasib produced an unprecedented doubling of overall survival versus chemotherapy. If confirmed in full peer-reviewed data, this could establish daraxonrasib as a new standard-of-care and accelerate further development of RAS-targeted therapies in PDAC.

Cancer discovery · (2026) · View on PubMed ↗

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Neurodegeneration biomarkers & risk factors (AD/PD/ALS/FTLD)

Serum neurofilaments for motoneuron and dementia diseases: a German multicenter cohort study.

This German multicenter cohort study measured serum neurofilament light (sNfL) and neurofilament heavy (sNfH) using immunoassays in patients with amyotrophic lateral sclerosis (ALS) and multiple dementia/FTLD subtypes (n=340 in the FTLD Consortium and n=290 in a single-center cohort). sNfH diagnostic performance was systematically evaluated relative to sNfL across neurodegenerative disorders, addressing the previously limited evidence base for sNfH. The results support more informed use of serum neurofilament biomarkers for differential diagnosis and disease characterization in ALS and dementia.

Barba L, Steinacker P, Halbgebauer S et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Associations of Anthropometry Measures Across 35 Years With Late-Life Plasma P-tau217 and Dementia: The HUNT Study.

This study examined life-course adiposity—waist-to-height ratio (WtHR) and body mass index (BMI)—in participants aged ≥70 years from the Norwegian Trøndelag Health Study (HUNT4; 2017–2019) and related it to plasma p-tau217 and biomarker-verified Alzheimer disease (AD) dementia. Higher WtHR/BMI across the life course was associated with plasma p-tau217 levels and with AD dementia status based on biomarker criteria. These findings support central/general adiposity as a modifiable risk factor that may influence late-life AD pathology measurable by plasma p-tau217.

Zotcheva E, Strand BH, Sunde A et al. · Neurology · (2026) · View on PubMed ↗

Proteomic signatures of early retinal neurodegeneration in type 2 diabetes mellitus.

This multi-cohort prospective observational study used high-throughput plasma proteomics combined with longitudinal optical coherence tomography (OCT) to identify circulating protein signatures of diabetic retinal neurodegeneration (DRN) in people with type 2 diabetes mellitus. The authors reported distinct plasma proteomic patterns that tracked with OCT-defined early DRN and enabled development of a clinically usable DRN risk prediction system. This provides candidate blood-based biomarkers and a potential individualized tool for earlier detection and risk stratification of neurodegenerative diabetic retinal disease.

Li H, Zhu Z, Yang S et al. · PLoS medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Planimetric and Linear MRI Markers for Progressive Supranuclear Palsy Classification: A Large Multicohort International Study.

This large multicohort international study evaluated planimetric and linear MRI markers to classify progressive supranuclear palsy (PSP) versus Parkinson disease and other parkinsonisms using data from prospective studies spanning 2006–2024. The key finding was that specific planimetric/linear measurements—particularly an optimized linear marker derived from the midbrain/pons-related metrics—improved discrimination of PSP from other parkinsonisms (full performance metrics truncated in the abstract). Clinically, better MRI-based differentiation could reduce diagnostic uncertainty and improve patient stratification for trials and management.

Quattrone A, Bianco MG, Vescio B et al. · Radiology · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroinflammation, innate immunity & inflammasomes in CNS

Stress, stress systems, and Alzheimer’s disease.

This review examined how stress and stress-response systems contribute to Alzheimer’s disease (AD) initiation, progression, and outcomes, integrating epidemiologic evidence with experimental mechanistic findings. It highlights that stress hormones can directly drive core AD pathology—amyloid beta and tau aggregation, neuroinflammation, and neurodegeneration—while brain circuits that regulate stress are themselves selectively vulnerable to early AD degeneration. The synthesis supports stress biology as a modifiable risk factor and a potential target for interventions aimed at slowing AD-related neurodegeneration.

Eberly SG, Phumsatitpong C, Munro CE et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

Pharmacologic Modulation of ARID3A with Rimegepant Reactivates Type I Interferon Signaling and Sensitizes Triple-Negative Breast Cancer to PD-1 Blockade.

This study examined whether pharmacologic modulation of the transcription factor ARID3A using rimegepant can reactivate type I interferon signaling and sensitize triple-negative breast cancer (TNBC) to PD-1 blockade in vivo. ARID3A modulation increased innate immune sensing and type I interferon pathway activity, leading to enhanced dendritic-cell activation and greater CD8+ T-cell infiltration and cytotoxicity, thereby sensitizing resistant tumors to PD-1 inhibitors. Clinically, this suggests a potential combination strategy of rimegepant with PD-1 blockade to convert immune-cold TNBC into an immune-active state.

Zhou T, Zhu Y, Zeng C et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Non-transcriptional activity of IRF3 promotes liver fibrosis and stress granule assembly via a dsRNA-TLR3-dependent pathway in hepatic stellate cells.

This study examined the role of non-transcriptional IRF3 activity in hepatic stellate cells in promoting liver fibrosis and stress granule assembly, using mouse models with IRF3 transcriptional activity selectively disrupted (Irf3S1/S1) and IRF3-deficient controls (Irf3−/−), plus hepatic stellate cell–specific Irf3 deletion (Lrat-Irf3). It found that chronic CCl4 and choline-deficient diets induced fibrosis in mice with only non-transcriptional IRF3 activity but not in Irf3−/− mice, and that IRF3 non-transcriptional signaling promotes fibrosis via a dsRNA–TLR3-dependent pathway leading to stress granule assembly. These results identify a specific innate immune axis (dsRNA–TLR3) downstream of IRF3 that could be targeted to limit fibrogenesis.

Travers J, Zhang Y, Cajigas-Du Ross CK et al. · Hepatology (Baltimore, Md.) · (2026) · View on PubMed ↗

The Peri-necrotic Niche of Glioblastoma Drives Tumor-associated Macrophage Polarization and Immunosuppression via Podoplanin-mediated CLEC5A Activation.

This study examined how the peri-necrotic niche in glioblastoma (IDH-wildtype) drives tumor-associated macrophage (TAM) polarization and immunosuppression, focusing on Podoplanin-mediated activation of CLEC5A. Using an RCAS/tv-a GBM model with bone marrow transplant (and related mechanistic experiments), it found that CLEC5A is preferentially expressed in hypoxic, peri-necrotic TAMs and that Podoplanin signaling activates CLEC5A to promote an immunosuppressive TAM phenotype with increased immunoregulatory cytokine secretion. Clinically, it identifies a specific macrophage-activation axis (Podoplanin→CLEC5A) that could be targeted to disrupt immunosuppression in GBM.

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

Decoding neuroinflammation: the critical role of NLRP3 inflammasome in Alzheimer’s disease.

This review studied the NLRP3 inflammasome’s role in Alzheimer’s disease (AD) pathogenesis, focusing on how innate immune activation in the brain links to amyloid-β (Aβ) plaques, tau pathology, and neuroinflammation. It found that multiple triggers—including Aβ, oxidative stress, mitochondrial dysfunction, ion fluxes, and gut dysbiosis—can activate NLRP3 via pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), driving downstream inflammatory signaling. These mechanistic insights support NLRP3 inflammasome signaling as a potential therapeutic target to modulate neuroinflammation in AD.

Chaudhary B, Kumari S, Sharma P et al. · Inflammopharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

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Genetic testing, variant interpretation & clinical genomics (epilepsy, HLA, etc.)

HLA matching in contemporary haematopoietic cell transplantation: Recommendations from the EBMT Practice Harmonisation and Guidelines Committee.

This EBMT guideline/recommendations paper reviewed contemporary evidence on the clinical relevance of HLA matching in allogeneic hematopoietic cell transplantation (HCT), considering modern HLA typing technologies and current graft-versus-host disease (GvHD) prophylaxis strategies. The key conclusion is that HLA mismatch remains associated with worse outcomes, but the magnitude and practical implications need to be interpreted in light of advances in typing, supportive care, and GvHD prevention. These harmonized recommendations aim to standardize HLA matching decisions in current HCT practice to improve survival and reduce GvHD.

Arrieta-Bolaños E, Lima ACM, Andreani M et al. · Bone marrow transplantation · (2026) · View on PubMed ↗ · Free PDF ↗

Pediatric epilepsy surgery: Global survey of referral and presurgical evaluation practices.

This global survey studied referral and presurgical evaluation practices for pediatric epilepsy surgery across 61 epilepsy surgery programs in 29 countries using ILAE Pediatric Epilepsy Surgery Task Force group-level data. It found that data were available for 2427 patients treated in 2023, with a mean age at surgery of 9.1±4.9 years, and it characterized regional differences in how children and adolescents are evaluated and referred for surgery. The significance is that it provides an up-to-date international benchmark to identify gaps and standardize presurgical pathways for pediatric epilepsy surgery.

Ramantani G, Cross JH, Cserpan D et al. · Epilepsia · (2026) · View on PubMed ↗ · Free PDF ↗

ACMG/AMP variant classification specifications from the ClinGen Epilepsy Sodium Channel Variant Curation Expert Panel.

This ClinGen expert panel work adapted ACMG/AMP sequence-variant classification specifications for epilepsy genes SCN1A, SCN2A, SCN3A, SCN8A, and SCN1B, using clinical, bioinformatic, and functional evidence. In a pilot on 37 variants spanning pathogenic, benign, and VUS categories, the panel produced gene-specific, standardized criteria for variant interpretation. The resulting specifications improve consistency and clinical reliability of genetic diagnosis for SCN-related epilepsies and neurodevelopmental disorders.

Smith L, Bonkowski E, Prentice A et al. · Genetics in medicine : official journal of the American College of Medical Genetics · (2026) · View on PubMed ↗

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DNA repair & genome stability as therapeutic targets

DREAM repressive activity links somatic mutation, lifespan and disease.

This study examined how DREAM complex repressive activity affects lifetime somatic mutation burden, lifespan, and age-related disease pathology. By profiling DREAM-associated transcriptional repression across a single-cell atlas of 21 mouse tissues and integrating these data with somatic mutation rates, the authors found that niches with lower DREAM-associated activity had decreased mutation rates and that DREAM-associated activity predicted lifespan and age-related disease pathology. These findings link a DNA-repair transcriptional repressor network to long-term genomic stability and aging outcomes, suggesting DREAM activity as a potential lever for modulating age-associated disease risk.

Koch Z, Nandi SP, Licon K et al. · Nature aging · (2026) · View on PubMed ↗

Nucleophagy removes cytotoxic trapped PARP1.

The authors studied how PARP inhibitor–induced trapped PARP1 is cleared from chromatin, focusing on nucleophagy mechanisms in cancer cells exposed to PARP inhibitors (PARPi). They found that trapped PARP1 is removed via nucleophagy mediated by the selective autophagy receptor TEX264 and its partner segregase p97/VCP, which orchestrates the clearance process. This mechanistic insight explains how cells can adapt to PARPi and identifies nucleophagy components as potential targets to modulate PARPi sensitivity.

Hoslett G, Tribble S, Lascaux P et al. · Nature cell biology · (2026) · View on PubMed ↗ · Free PDF ↗

Structures of human telomerase with BIBR1532 reveal novel mechanism of inhibition.

This structural biology study determined cryo-electron microscopy structures of human telomerase bound to the selective small-molecule inhibitor BIBR1532. They reported nine cryo-EM structures and found that BIBR1532 binds a previously unknown pocket between the TERT finger and palm, inhibiting each step of telomerase activity. The structure-based mechanism advances rational design of next-generation telomerase inhibitors for oncology.

Wang Y, Liu B, He Y et al. · Nature chemical biology · (2026) · View on PubMed ↗ · Free PDF ↗

Multi-omics and artificial intelligence for precision drug discovery and potential clinical applications.

This article reviewed how integrating multi-omics data (genome-wide association studies, transcriptomics, proteomic interaction mapping, and metabolomics) with artificial intelligence can accelerate precision drug discovery and support clinical translation. It highlights that deep learning and other AI approaches can extract latent patterns and build predictive models from complex biological datasets. The significance lies in providing a conceptual framework for using multi-omics–AI pipelines to improve target identification, biomarker discovery, and drug development decision-making.

Liu Y, Zhu K, Peng W et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

A cytosolic IF1 reporter enables real-time visualization of severe mitochondrial membrane damage.

This study developed and characterized MAI-1, a genetically encoded cytosolic IF1-based reporter, in C. elegans and validated cytosolic IF1 variants in mammalian-relevant injury paradigms to visualize severe mitochondrial membrane damage in real time. MAI-1 rapidly and irreversibly translocated to severely damaged mitochondria within milliseconds, enabling detection of catastrophic mitochondrial injury across diverse damage models. This provides a conserved, fast imaging tool to study mitochondrial catastrophe mechanisms and to screen or evaluate interventions that prevent severe mitochondrial membrane damage.

Gao E, Guan L, Zhang K et al. · The Journal of cell biology · (2026) · View on PubMed ↗ · Free PDF ↗

De Novo Design of Near-Infrared Fluorescence-Activating Proteins.

This study developed a de novo computational protein design and organic synthesis workflow to create near-infrared (NIR, 800–1000 nm) and shortwave infrared (SWIR, 1000–2000 nm) fluorescence-activating proteins. The key finding was successful de novo design of proteins that specifically bind synthetic merocyanine dyes and form a Schiff base cofactor to activate long-wavelength fluorescence. This expands the toolkit for deep-tissue and high-contrast fluorescence imaging by enabling new protein probes in optical windows where suitable genetically encoded reporters are scarce.

Liu Y, Arús BA, Mishra K et al. · Journal of the American Chemical Society · (2026) · View on PubMed ↗

Therapeutic targeting of DNA repair pathway dysregulation in aging, cancer, and neurodegeneration.

This review synthesized evidence on therapeutic targeting of DNA repair pathway dysregulation across aging, cancer, and neurodegeneration, covering base excision repair, nucleotide excision repair, mismatch repair, homologous recombination, and end-joining pathways. It concluded that oxidative stress, replication stress, telomere dysfunction, mitochondrial injury, and persistent DNA damage response signaling remodel DNA repair in ways that can be therapeutically exploited. Scientifically, it frames DNA repair as a shared vulnerability and highlights pathway-specific targets for translational drug development across multiple disease areas.

Kumar V, Kashif M, Singh V et al. · Expert opinion on therapeutic targets · (2026) · View on PubMed ↗

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Cell death mechanisms (ferroptosis, necroptosis, NETosis) & inflammation

Spermine is an endogenous iron chelator that inhibits ferroptosis.

This study investigated whether spermine, a polyamine, functions as an endogenous iron chelator to regulate ferroptosis in hepatocellular carcinoma models, focusing on the role of aldehyde dehydrogenase 18 family member A1 (ALDH18A1) in spermine synthesis. Using metabolomics, stable isotope tracing, and biophysical interaction assays with Fe2+, the authors found that spermine directly suppresses ferroptosis by limiting iron availability and lipid peroxidation, and that ALDH18A1 promotes an alternative glutamine-dependent de novo spermine pathway that drives this protective effect. These findings suggest targeting the ALDH18A1–spermine axis could be a host-metabolic strategy to modulate ferroptosis in liver cancer.

Li M, Yu X, Ouyang S et al. · Nature · (2026) · View on PubMed ↗

NETosis associates with human TB lung tissue destruction and disease pathogenesis.

This study investigated whether NETosis contributes to tuberculosis (TB) lung tissue destruction and disease pathogenesis in human samples. Using proteomics on human TB granuloma tissue to identify neutrophil-associated proteins enriched in necrotic regions of caseous and cavitary granulomas, and validating findings by immunohistochemistry (including markers such as myeloperoxidase, MPO), the authors linked NETosis-associated signatures to pathological lung damage. These results support NETosis as a potential host-directed therapy target to limit TB-associated tissue destruction.

Fisher KL, Mpotje T, Nargan K et al. · EMBO molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Explosive cytotoxicity of ruptoblasts bridges hormone surveillance and immune defense.

Researchers studied cytotoxic immunity in regenerative planarian flatworms by identifying a new glandular cell type, “ruptoblasts,” and testing how the hormone activin triggers their explosive cell death (“ruptosis”). They found that activin-induced ruptosis can be initiated by activin exposure via protein injection, genetic chimerism, or bacterial infection and results in rapid discharge of diffusible cytotoxic agents that kill nearby cells, bacteria, and even mammalian cells. This work links hormone surveillance to immune defense mechanisms, suggesting a conserved principle for how endocrine signals can rapidly orchestrate cytotoxic responses.

Chai C, Sultan E, Sarkar SR et al. · Cell · (2026) · 1 citations · View on PubMed ↗

Reductive death is averted by a conserved de novo lipogenic switch.

This mechanistic study investigated how biguanides (including metformin) cause toxicity when de novo lipogenesis is impaired, focusing on a conserved de novo lipogenic switch that protects against “reductive death.” The key finding was that biguanide accumulation of damaging reducing equivalents leads to NADPH toxicity, catastrophic elevation of NADH/GSH reducing equivalents, and accelerated death, which can be averted by activating de novo lipogenesis. Scientifically, it reframes metformin’s safety assumptions by identifying a specific metabolic vulnerability and a protective lipogenic defense pathway.

Ahsan FM, Rotti JF, Yerevanian AI et al. · Molecular cell · (2026) · View on PubMed ↗

NAT10-dependent N4-acetylcytidine reprograms R-loops and promotes cancer stem cell growth.

This study investigated how nociceptive neurons regulate neutrophil extracellular trap (NET) formation in neuroinflammation relevant to chronic pain, focusing on MLKL (a necroptosis effector) and histone H3 release. It found that MLKL is constitutively nuclear in nociceptive neurons and binds histone H3, and that inflammatory disruption of the MLKL/H3 interaction triggers cytoplasmic MLKL translocation and extracellular histone H3 that promotes NETs, hyperalgesia, and likely signaling via P2X7 and TLR4. Scientifically and therapeutically, it links a necroptosis-associated pathway to neuron-driven NET formation and identifies MLKL as a potential target to reduce pain-associated neuroinflammation.

Wu X, Wang D, Taori S et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Ferroptosis promotes aortic stenosis through 5-lipoxygenase.

This study examined whether ferroptosis drives aortic stenosis via 5-lipoxygenase (5-LOX) and validated translational relevance across human samples and models. Using bulk and single-cell transcriptomics, whole-mount histology, immunohistochemistry, and primary human valvular interstitial cell models from 212 surgical aortic valves, it linked ferroptosis-associated changes to 5-LOX and confirmed ferroptosis and valve thickening in a doxorubicin-induced ferroptosis mouse model. The work positions the ferroptosis–5-LOX axis as a druggable pathway for developing pharmacologic therapies for calcific aortic valve disease.

Qin Z, Haftbaradaran Esfahani P, Pawelzik SC et al. · European heart journal · (2026) · View on PubMed ↗

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Cardiovascular repair, remodeling & device/biomaterials

Exploring the therapeutic potential of GLP-1 receptor agonists in pulmonary arterial hypertension.

This article explored the therapeutic potential of glucagon-like peptide-1 receptor agonists (GLP-1RAs) for pulmonary arterial hypertension (PAH), a subtype of pulmonary hypertension characterized by vascular remodeling, inflammation, and fibrosis. It summarizes emerging rationale that GLP-1RAs may address metabolic and inflammatory drivers of PAH, particularly in patients with cardiovascular comorbidities where outcomes remain suboptimal despite established therapies (endothelin, nitric oxide, prostacyclin, and activin signaling via sotatercept). The review positions GLP-1RAs as candidate host-directed metabolic therapies that warrant clinical investigation in PAH.

Aguado B, Lacoste-Palasset T, Ruffenach G et al. · ERJ open research · (2026) · View on PubMed ↗ · Free PDF ↗

Magnetoelectric microrobots for spinal cord injury regeneration.

The study developed magnetoelectric biohybrid microrobots (“NPCbots”) by integrating human induced pluripotent stem cell–derived neural progenitor cells (NPCs) with magnetoelectric nanoparticles, and evaluated them in a zebrafish spinal cord injury model. Wireless magnetic navigation plus non-invasive neuronal stimulation improved regenerative outcomes by supporting NPC graft survival and controlled functional integration after injury. This provides a translational platform combining cell therapy with controllable neuromodulation for spinal cord injury regeneration.

Ye H, Zang J, Zhu J et al. · Nature materials · (2026) · 3 citations · View on PubMed ↗ · Free PDF ↗

A wearable non-invasive sonogenetic pacemaker.

Researchers engineered a wearable, non-invasive ultrasound pacemaker that activates engineered sonogenetic ion channels (MscL-G22S) to pace cardiomyocytes, testing performance in transfected human cardiomyocytes in vitro and in rats in vivo. Ultrasound stimulation produced spatiotemporally precise pacing with synchronized calcium signaling in vitro and non-invasive cardiac pacing in rats with sub-millimeter spatial precision and up to 9 Hz frequency control. This suggests a potentially safer alternative to implanted pacemakers by enabling external, wireless control of cardiac rhythm via sonogenetics.

Gong C, Lu G, Liu B et al. · Nature biomedical engineering · (2026) · View on PubMed ↗

Agreement of minimally invasive pulse wave analysis with pulmonary artery and transpulmonary thermodilution cardiac output measurements in perioperative and intensive care medicine: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated agreement between minimally invasive pulse wave analysis (cardiac output/cardiac index) and reference cardiac output methods—pulmonary artery thermodilution or transpulmonary thermodilution—in adult perioperative and intensive care patients. Pooled estimates quantified percentage error, mean difference, and 95% limits of agreement across studies using random-effects models. The findings inform how reliably pulse wave analysis can substitute for thermodilution-based cardiac output monitoring in high-risk surgical and critically ill populations.

Flick M, Müller DX, Bergholz A et al. · British journal of anaesthesia · (2026) · View on PubMed ↗ · Free PDF ↗

Haemodynamic Responses to Sotatercept and Parenteral Prostacyclins in Pulmonary Arterial Hypertension Patients.

This retrospective study evaluated haemodynamic responses in pulmonary arterial hypertension (PAH) patients who sequentially received parenteral prostacyclins (with or without oral PAH therapies) followed by sotatercept in the French early access program. Across 62 patients, the study tracked changes in cardiac index and stroke volume index alongside pulmonary vascular resistance to compare response patterns between prostacyclins and sotatercept. The findings help clinicians anticipate differing haemodynamic trajectories when transitioning from prostacyclin-based therapy to sotatercept in PAH.

Genecand L, Boucly A, Beurnier A et al. · The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · (2026) · View on PubMed ↗

Personalized automatic management of tracheal cuff pressure and subglottic secretions drainage to prevent pneumonia in critically ill intubated patients. The MICROINHALO multicenter randomized controlled trial.

This multicenter cluster-randomized trial studied whether personalized automatic management of endotracheal tube cuff pressure (Pcuff) using exhaled CO2 measurement combined with automatic subglottic space drainage (SSD) can prevent pneumonia by reducing tracheal colonization in adult intubated ICU patients. It found that the MICROINHALO intervention was tested against conventional manual Pcuff management and manual SSD, with the primary endpoint being bacterial tracheal colonization (>10^3 CFU/mL) on day 3 after intubation. The trial is significant because it evaluates device-based, automated airway management strategies to lower early bacterial colonization risk and potentially prevent ventilator-associated pneumonia.

De Pascale G, Cutuli SL, Vargas M et al. · Intensive care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Myeloid Piezo1 Drives Cardiac Repair Through Orai1-Rac1-Dependent Efferocytosis.

This mouse study tested whether myeloid-specific Piezo1 regulates cardiac repair after myocardial infarction through Orai1–Rac1-dependent efferocytosis. In Piezo1ΔLysM mice subjected to left anterior descending coronary artery ligation, impaired efferocytosis was linked to worse post-infarction remodeling, while mechanistic experiments supported a Piezo1→Orai1→Rac1 pathway controlling macrophage clearance of apoptotic cells. These findings identify myeloid Piezo1 as a potential therapeutic target to improve cardiac healing after infarction.

Liu S, Xu H, Deng B et al. · Circulation research · (2026) · View on PubMed ↗

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Aging, circadian biology & lifestyle interventions

Plasma antioxidant capacity as a predictor of mortality in critically ill patients.

This prospective multicenter observational study assessed whether plasma total antioxidant capacity measured by the Ferric Reducing Antioxidant Power (FRAP) assay predicts mortality in 464 critically ill postoperative patients in Spanish ICUs. FRAP levels were measured within 24 hours after surgery or after diagnosis of sepsis or shock, and the study evaluated their prognostic value for outcomes. If validated, FRAP-based antioxidant capacity could serve as an early biomarker to risk-stratify critically ill patients and potentially guide antioxidant-related interventions.

Cobo-Zubia R, Prieto-Utrera RD, Álvarez-Bardón M et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Time-restricted feeding extends healthspan in both sexes and lifespan in male C57BL/6 J mice.

This experiment tested whether time-restricted feeding (TRF) improves healthspan and lifespan in both sexes and whether effects depend on TRF window length in C57BL/6J mice. In 264 male and 264 female mice fed regular chow, 12-hour and 8-hour nightly TRF improved multiple health measures (including behavioral rhythmicity, body weight/composition, frailty, and disease onset), with the 8-hour TRF group showing the strongest benefits and voluntary caloric restriction in addition to time restriction. The study supports circadian-aligned feeding as a non-obesogenic dietary intervention that can extend healthspan and lifespan, informing translational strategies for metabolic and aging interventions.

Iiams SE, Skinner NJ, Wight-Carter M et al. · Nature aging · (2026) · View on PubMed ↗

Exercise attenuates obesity-related cognitive and sleep-circadian dysfunctions by attenuating neuroinflammation via JAK/STAT in sex and age specific manner.

The study used Drosophila melanogaster to test whether exercise mitigates obesity-related cognitive decline and sleep–circadian dysfunction in genetic obesity models, examining sex- and age-specific responses and focusing on neuroinflammation pathways including JAK/STAT. Exercise attenuated obesity-associated cognitive and circadian impairments by reducing neuroinflammation via JAK/STAT signaling in a sex- and age-dependent manner. These findings support exercise as a mechanistically actionable lifestyle intervention for obesity-driven brain and circadian dysfunction and suggest JAK/STAT as a targetable pathway for personalized risk reduction.

Yadav A, Barkley M, Watson JC et al. · International journal of obesity (2005) · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting hypothalamic SIK3 to promote weight loss and improve glycemic control in mice.

The study investigated whether hypothalamic Salt-Inducible Kinase 3 (SIK3) in orexigenic neuropeptide Y (NPY) neurons regulates body weight and glucose metabolism in mice, including using the pharmacological SIK3 inhibitor GLPG3970 in diet-induced obese animals. Genetic inactivation of SIK3 in NPY neurons reduced food intake, increased energy expenditure, promoted white adipose tissue browning, and protected against high-fat diet-induced obesity, while GLPG3970 similarly improved weight and metabolic outcomes. These findings are significant because they nominate hypothalamic SIK3 as a mechanistic target for anti-obesity and glycemic-control therapies.

Onda DA, Yang CH, Goldsmith C et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Nociceptor circadian clock genes control excitability and pain perception in mice in a sex- and time-dependent manner.

This work examined how circadian clock genes in nociceptors (dorsal root ganglia, DRG) control excitability and pain perception in mice, assessing sex- and time-dependent effects. DRGs showed time- and sex-dependent expression of core clock genes, and electrophysiology/optogenetic experiments using Nav1.8-expressing nociceptors demonstrated that male nociceptor excitability and pain-related responses vary across the circadian cycle. The study is important because it links peripheral nociceptor clock biology to sex- and time-dependent pain, suggesting chronobiology as a lever for improving pain management.

Brécier A, Bannerman CA, Xie YF et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

A Rras2-BMPR2 feedback loop sustains osteogenesis and represents a therapeutic target for osteoporosis.

This study tested the role of Ras-related protein 2 (Rras2) in bone homeostasis by analyzing Rras2 deficiency in mice and defining the molecular pathway controlling osteogenesis, focusing on BMP signaling and BMPR2 stability. Rras2 loss caused osteopenia, reduced bone strength, and impaired osteogenic differentiation, while mechanistically Rras2 sustained BMP signaling by blocking Smurf1-dependent ubiquitination and degradation of BMPR2. The results are clinically significant because they identify the Rras2–BMP axis as a therapeutic target for osteoporosis.

Yang R, Li M, Xue Q et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Decreased degree of adipocyte differentiation in visceral adipose tissue contributes to metabolic dysfunction-associated steatotic liver disease.

Using single-nucleus RNA sequencing of human adipose tissue biopsies, this study assessed whether impaired adipocyte differentiation in visceral adipose tissue (VAT) contributes to metabolic dysfunction-associated steatotic liver disease (MASLD). The authors found that the predicted degree of VAT adipocyte differentiation was decreased in individuals with MASLD (with a smaller effect in subcutaneous adipose tissue, SAT), and that regional VAT adipocyte differentiation gene-set variants explained additional variance in MASLD-related features. This is significant because it connects human depot-specific adipocyte differentiation programs to MASLD risk and highlights potential molecular targets for intervention.

Gelev KZ, Lee SHT, Alvarez M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Long-term resistance training with all-cause and cause-specific mortality: assessing dose-response and joint associations with aerobic physical activity.

This prospective cohort analysis studied whether long-term resistance training is associated with lower all-cause and cause-specific mortality and whether effects show dose-response and joint associations with aerobic activity in participants from the Health Professionals Follow-up Study and Nurses’ Health Studies (total n=147,374). Using Cox proportional hazards models with repeated questionnaire-based assessments of resistance and aerobic exercise, the study estimated hazard ratios for mortality outcomes across resistance-training duration categories and in combination with aerobic activity. The results clarify the mortality benefit of resistance training and help refine exercise prescriptions alongside aerobic exercise.

Zhang Y, Lee DH, Rezende LFM et al. · British journal of sports medicine · (2026) · View on PubMed ↗

Liver stiffness dynamics in European populations (LiverScreen): a longitudinal, multicentre, prospective, population-based cohort study.

The LiverScreen longitudinal, multicentre prospective cohort study followed adults (≥18 years) from three European populations—Barcelona (Spain), Odense (Denmark), and Rotterdam (Netherlands)—to model liver stiffness measurement (LSM) dynamics over time and identify risk factors for clinically significant changes. The study found measurable long-term LSM trajectories that differed by population and were associated with specific risk factors for clinically significant worsening or improvement. Clinically, this supports using serial LSM to refine liver fibrosis screening and risk stratification beyond single time-point measurements.

Pustjens J, Bech KT, Pera G et al. · The lancet. Gastroenterology & hepatology · (2026) · View on PubMed ↗

The effects of anti-osteoporotic medication on fracture healing and outcomes: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluated how anti-osteoporotic drugs—bisphosphonates and teriparatide—affect fracture healing outcomes in adults with acute fractures. The key finding was that these medications did not meaningfully worsen fracture union and were assessed for effects on complications and patient-reported outcomes, addressing concerns that antiresorptives might delay healing. Scientifically and clinically, the results help guide osteoporosis medication choice around the time of fracture to optimize both healing and long-term fracture prevention.

Agarwal N, Bell KR, Ross LE et al. · The lancet. Healthy longevity · (2027) · View on PubMed ↗ · Free PDF ↗

Molecular cues from distinct neuron classes drive differential myelination in the neocortex.

This study used single-cell mapping of oligodendrocyte lineage cells purified from different neocortical layers across developmental stages to test what drives layer-specific myelination. It found that each cortical layer contains a similar set of oligodendrocyte classes, with differences mainly in maturation-state proportions, and that signals from distinct pyramidal neuron classes control oligodendrocyte maturation and the resulting myelin distribution. These findings identify neuron-derived ligand–receptor cues as key regulators of cortical myelination, informing mechanisms of developmental circuit maturation.

Domínguez-Iturza N, Jokhi V, Kim K et al. · Developmental cell · (2026) · View on PubMed ↗

NMI Regulates Adipose Adaptive Thermogenesis Through TLR4/IRF3 Signaling to Promote Obesity.

This study examined the role of N-Myc and STAT interactor (NMI; gene Nmi) in adipose adaptive thermogenesis and obesity, using mouse models of diet-induced obesity and adipocyte stress/inflammatory stimulation. It found that NMI suppresses adaptive thermogenesis via TLR4/IRF3 signaling, and that genetic ablation of Nmi protects mice from diet-induced obesity by enhancing brown adipose tissue thermogenesis and white adipose tissue browning. These results are significant because they identify NMI–TLR4/IRF3 as a mechanistic pathway that could be targeted to improve obesity-related metabolic dysfunction.

Li TT, Zhao XY, Zhang M et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Pre-teriparatide anti-osteoporosis medication therapy and fracture-related hospitalization in patients at very high fracture risk.

This nationwide cohort study evaluated whether prior anti-osteoporosis medication (AOM) use affects fracture-related hospitalization in patients at very high fracture risk who subsequently initiated teriparatide. It found that prior bisphosphonate use was associated with decreased fracture and spinal fracture-related hospitalization, denosumab showed no clear decrease, and long-term denosumab (≥3 years) was associated with increased spinal fracture-related hospitalization after transitioning to teriparatide. The findings are clinically significant for sequencing osteoporosis therapies to reduce fracture risk when moving from antiresorptives to teriparatide.

Fu SC, Lu YC, Sie NH et al. · Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · (2026) · View on PubMed ↗

Nutrition support in the ICU: current evidence and evolving standards.

This review studied current evidence and evolving standards for nutrition support in the ICU, focusing on how macronutrient delivery should be tailored across phases of critical illness. It found that traditional early full nutritional replacement may be harmful due to risks such as overfeeding, refeeding syndrome, impaired autophagy, and metabolic intolerance, and that low-calorie/low-protein strategies during the first week—especially in mechanically ventilated patients—are increasingly considered. The review is significant because it informs safer, more physiologically aligned nutritional targets to reduce muscle wasting and metabolic complications in critically ill patients.

Peake SL, Ridley EJ, Reignier J · Intensive care medicine · (2026) · View on PubMed ↗

BMI-mediated association between pulmonary function and bone mineral density moderated by age: Integrated Mendelian randomisation and cross-sectional study.

Using NHANES data from 10,944 participants, this integrated Mendelian randomisation and cross-sectional analysis tested whether pulmonary function (FEV1/FVC) is associated with bone mineral density (BMD) and whether age moderates this relationship. The study found that the pulmonary function–BMD association varied by age, indicating effect modification rather than a uniform relationship across the lifespan. Clinically, this supports age-stratified risk assessment for osteoporosis in people with COPD-related airflow limitation.

Yi Z, Jiang Q, Jiang Y et al. · Pulmonology · (2026) · View on PubMed ↗ · Free PDF ↗

Lifestyle-Induced Visceral Fat Loss as a Key Target for Durable Cardiometabolic Health: MRI-Assessed 5- and 10-Year Follow-Up After 2 Clinical Trials.

This MRI-based follow-up study assessed whether lifestyle-induced visceral fat loss predicts durable cardiometabolic health over 5 and 10 years after participants completed the CENTRAL and DIRECT-PLUS randomized clinical trials. It evaluated long-term cardiometabolic profiles in relation to changes in abdominal and ectopic fat achieved during the 18-month interventions. The findings support visceral fat loss as a key target for sustained cardiometabolic benefit, informing long-term prevention strategies.

Klein H, Alufer L, Goldberg Toren DT et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗

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