PubMed Trending Research Digest — July 26, 2026

Automated digest · 96 articles · 15 research areas · July 26, 2026

Overview

Across this week’s papers, a dominant theme is mechanism-driven precision: multiple studies connect specific molecular “levers” to disease behavior and treatment response. In oncology, work spans metabolic control of metastasis and drug resistance (e.g., ADSL–fumarate–SLC7A11/Scrib-Rictor axes; 5-FU metabolite–GPCR signaling bias), targeted pathway inhibition (KRAS-pathway precision in pancreatic cancer; EGFR dimer structural regulation; EGFR-TKI resistance frameworks), and immune-evasion biology (CD47-targeting NK engagers, CSF-1R blockade strategies, and UFMylation inhibition that reprograms glioblastoma microenvironments). Complementing these, multi-omics/proteogenomic studies show how somatic driver alterations remodel systems like the ubiquitin–proteasome network at the protein level—highlighting why transcriptomics alone can miss actionable biology.

A second major cluster centers on neurodegeneration and neuroinflammation, with strong emphasis on blood-based biomarkers and early mechanistic links. Plasma phosphorylated tau and protein signatures (GFAP and others) are advanced for differentiating dementia subtypes and staging, while reviews and scoping work support standardizing endpoints such as blood NfL. Mechanistic studies also broaden the inflammatory landscape: microglial state diversity is reframed beyond simple M1/M2 models, complement activation appears early in synucleinopathy, and cardiomyocyte-derived extracellular vesicles are implicated in hypothalamic microglial activation in HFpEF.

Finally, several clinical and translational studies address respiratory, cardiovascular, and critical-care decision-making. Trials and reviews refine interventions ranging from prone positioning in ARDS and IL-33/TEZEL (endotype-targeted) therapy in CRSwNP to long-acting RSV prevention and high-dose influenza vaccination in older adults. In parallel, critical-care evidence syntheses (ECMO plus hemoperfusion; bicarbonate in severe metabolic acidemia) and perioperative strategies (immunonutrition, pain-management updates) underscore a broader push toward better patient selection, safer implementation, and measurable outcome improvements.

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Cancer Metabolism & Metastasis

α-fluoro-β-alanine functions as a β-arrestin1-biased ligand of S1PR2 to upregulate DPD expression in cancer cells.

This work identified α-fluoro-β-alanine (FBAL), a catabolite of the chemotherapeutic 5-fluorouracil (5-FU), as a β-arrestin1-biased ligand of sphingosine-1-phosphate receptor 2 (S1PR2) in colorectal cancer cells. The key finding was that FBAL activates phosphorylated S1PR2 via GRK6 recruitment, upregulates dihydropyrimidine dehydrogenase (DPD/DPD expression), and thereby drives 5-FU resistance. Clinically, it links a 5-FU metabolite to a specific GPCR signaling bias that could be targeted to overcome resistance.

Tan M, Shao H, Zhang X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondrial SLC25A46 Rewires Fatty Acid Oxidation to Promote Cell Proliferation and Ferroptosis Evasion in Ovarian Cancer by Stabilizing CACT.

This study investigated the role of the mitochondrial bridging protein SLC25A46 in ovarian cancer, focusing on how it rewires fatty acid oxidation to promote proliferation and evade ferroptosis by stabilizing CACT (carnitine-acylcarnitine translocase) and involving MARCHF5-related regulation. The key finding was that SLC25A46 was upregulated in ovarian cancer and functionally promoted tumor growth and ferroptosis evasion through CACT protection, increasing ATP and NADPH production via fatty acid oxidation. Scientifically, it identifies the SLC25A46–CACT axis as a mechanistic vulnerability that could be targeted to overcome ferroptosis resistance in ovarian cancer.

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

Inhibition of the Metalloproteinase ADAMTS5 Suppresses Colorectal Cancer Metastasis via the PEDF/Wnt/β-Catenin Pathway.

This mechanistic cancer study evaluated the role of the metalloproteinase ADAMTS5 in colorectal cancer (CRC) metastasis and tested pathway involvement in vitro and in vivo. It found that ADAMTS5 is upregulated in CRC tissues and that inhibiting ADAMTS5 suppresses CRC metastasis through the PEDF/Wnt/β-catenin signaling pathway. These results suggest ADAMTS5 as a therapeutic target and provide a specific signaling route (PEDF/Wnt/β-catenin) for how ADAMTS5 promotes metastatic progression in CRC.

Sun X, Zhang H, Hu Y et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗

ADSL drives fumarate mediated scrib-rictor complex formation to promote metastasis dissemination in triple-negative breast cancer.

This study investigated how the metabolic enzyme ADSL drives fumarate-mediated formation of the SLC7A11? (scrib-rictor) complex to promote metastasis dissemination in triple-negative breast cancer (TNBC) using untargeted metabolomics, chemoproteomic succination profiling, molecular interaction assays, and in vivo metastasis models. The authors found that ADSL-driven fumarate production promotes S? (scrib-rictor) complex assembly, thereby enhancing metastatic dissemination in TNBC. These findings identify an ADSL–fumarate–S? (scrib-rictor) axis as a mechanistic metabolic driver of TNBC spread and a potential therapeutic target.

Fan Y, He X, Deng W et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Activity-based proteomics analysis revealed that DNJ directly targeted ATP5F1 to alleviate high glucose induced cardiomyocyte injury.

This study used activity-based protein profiling (ABPP) to identify direct molecular targets of the natural alkaloid 1-deoxynojirimycin (DNJ) in cardiomyocytes subjected to high-glucose injury, focusing on mitochondrial injury relevant to diabetic cardiomyopathy (DCM). DNJ directly targeted ATP5F1 (ATP synthase subunit F1) and reduced high-glucose–induced cardiomyocyte injury. These data provide a specific DNJ–ATP5F1 target mechanism that could inform development of mitochondria-directed therapies for diabetic cardiomyopathy.

Li X, Chen Y, Yang H et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Immunotherapy & Immune Evasion

NOD1/2 signaling in macrophages drives adaptive immune resistance in cancer.

This work studied the role of NOD1/2 signaling in macrophages in adaptive immune resistance to cancer therapies, using murine tumor models and mechanistic perturbations. Genetic ablation of NOD1/2 or RIPK2 and pharmacologic inhibition of the pathway reduced resistance across multiple antitumor modalities, including immune checkpoint blockade, adoptive T-cell therapy, and cytotoxic chemotherapy. The findings identify NOD1/2–RIPK2 macrophage signaling as a therapeutic vulnerability to overcome treatment resistance.

Wei X, Yang L, Wang Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Phase 1/2 study of IMC-C103C, a T cell receptor bispecific (MAGE-A4×CD3) ImmTAC targeting MAGE-A4-expressing malignancies.

A phase 1/2 clinical study (IMC-C103C-101; NCT03973333) evaluated IMC-C103C, a T cell receptor bispecific ImmTAC targeting MAGE-A4×CD3, in HLA-A*02:01+ patients with previously treated advanced solid tumors. The trial assessed safety and preliminary anti-tumor activity using weekly intravenous dosing with step-up dosing and dose-escalation guided by the mTPI-2 method, alongside pharmacokinetics/pharmacodynamics and biomarker analyses. This design targets MAGE-A4-expressing malignancies and aims to establish early clinical activity and tolerability for this HLA-restricted bispecific therapy.

Sweis RF, Melero I, Davar D et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Beyond immune checkpoint blockade: T cell engagers and antibody-drug conjugates in cancer and autoimmune disease.

This review article examined next-generation immunotherapies beyond immune checkpoint blockade, focusing on T cell engagers (TCEs) and antibody-drug conjugates (ADCs) in cancer and immune-mediated inflammatory disorders (IMIDs). It reports that TCEs can redirect cytotoxic T cells to target cells independently of MHC restriction, while ADCs deliver cytotoxic payloads via receptor-mediated internalization, addressing limitations such as resistance and on-target toxicity. Scientifically, it frames how these modalities—and examples such as the CD47/SIRPα innate immune checkpoint—could expand therapeutic options for both malignancy and autoimmune disease.

Abdelaziz AM, Shokr MM · Biochemical pharmacology · (2026) · View on PubMed ↗

Therapeutic targeting of CD47 using a tri-specific NK cell engager to inhibit multiple myeloma.

This preclinical study investigated a tri-specific NK cell engager designed to therapeutically target CD47 signaling to inhibit multiple myeloma. The key finding was that engaging NK cells to block CD47/SIRPα-mediated immune evasion enhanced anti-myeloma activity and addressed resistance mechanisms associated with high CD47 expression. The scientific significance is that CD47-directed tri-specific NK engagers may provide a new immunotherapy platform for patients with refractory multiple myeloma.

Sumankan R, Sungwan P, Boonsatit N et al. · Cancer immunology, immunotherapy : CII · (2026) · View on PubMed ↗ · Free PDF ↗

TANGENT study design: a phase III, randomized study of emactuzumab for the treatment of tenosynovial giant cell tumors.

The TANGENT phase III randomized study evaluated emactuzumab, a CSF-1R inhibiting monoclonal antibody, in patients with tenosynovial giant cell tumors (TGCT) who were not adequately managed by surgery or had high post-surgical recurrence risk. The trial design targets tumor biology by inhibiting CSF-1R dimerization to reduce tumor-associated macrophage activity, with efficacy and safety assessed over the planned randomized treatment period. If successful, this would support a shorter, targeted systemic option for TGCT that could reduce reliance on long-term CSF-1R pathway inhibitors and their side effects.

Gelderblom H, Palmerini E, van de Sande M et al. · Future oncology (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

γδ T cells show distinct responses to CMV after stem cell transplantation.

This study examined how γδ T cells respond to cytomegalovirus (CMV) after allogeneic hematopoietic stem cell transplantation (aHSCT) by tracking clones over time. Using longitudinal single-cell RNA sequencing combined with paired T cell receptor (TCR) sequencing across five post-transplant time points, it found patient-specific expansion of non-Vγ9Vδ2 γδ T cell clones, particularly within Vδ1+ and Vδ3+ subsets, associated with differences in CMV reactivation status. The work is significant because it provides clonal-resolution insight into immune reconstitution after aHSCT, potentially informing monitoring and therapeutic strategies for CMV complications.

Sibbertsen F, Song Z, Ly C et al. · Journal of molecular medicine (Berlin, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Dual-targeting pharmacological UFMylation inhibition reprograms tumor and immune microenvironments to achieve long-term glioblastoma regression.

This study evaluated two small-molecule UFMylation inhibitors that target the UFMylation E3 ligase complex core protein DDRGK1—osimertinib (via a covalent mechanism) and CP-24 (non-covalent)—to determine their effects on tumor and immune microenvironments in glioblastoma models. It found that both compounds disrupt the DDRGK1–UFL1 interaction, globally suppress UFMylation, inhibit ER-phagy, and induce ER stress, leading to long-term glioblastoma regression with microenvironment reprogramming. The results are significant because they provide first-in-class pharmacological UFMylation inhibition strategies that may overcome therapeutic resistance by coupling ER-stress pathways to anti-tumor immune remodeling.

Tan P, Liu Z, Hu X et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Exosomes in cancer drug resistance: dual roles in therapy failure and emerging precision therapeutics.

This review discussed how tumor-derived exosomes contribute to cancer drug resistance while also serving as emerging tools for precision therapeutics, introducing the concept of an “exosome paradox.” The key finding is that exosomal cargo—including proteins such as P-gp and PD-L1, nucleic acids such as miR-21 and lncRNA H19, and lipids/metabolites—can activate pathways like PI3K/AKT and MAPK to drive therapy failure and immune evasion. The scientific significance is that it frames exosome targeting and exosome-based delivery as complementary strategies to overcome resistance and enable more precise cancer treatment.

Tegegne BA, Belew H, Teffera ZH et al. · Cancer cell international · (2026) · View on PubMed ↗ · Free PDF ↗

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Targeted Oncology (Kinases, Receptors, Precision Targets)

First CAR T-Cell Therapy Approved for Solid Tumors.

China studied satricabtagene autoleucel (satri-cel), a claudin 18.2–targeted CAR T-cell therapy, in patients with claudin 18.2-positive, HER2-negative gastric or gastro-esophageal junction cancer. The phase II trial reported that the CAR T cells increased progression-free survival and overall survival. This first solid-tumor CAR T approval is clinically significant but highlights the need for further research to improve CAR T effectiveness in solid tumors.

Cancer discovery · (2026) · View on PubMed ↗

Ligand regulation and function of preformed EGFR dimers.

This study used cryo-electron microscopy to determine the structural basis of ligand regulation and function of preformed epidermal growth factor receptor (EGFR) dimers. The key finding was a detailed structural view showing how preformed EGFR dimers are stabilized and regulated, refining the classic ligand-induced dimerization model for EGFR activation. Scientifically, this provides a mechanistic framework that can inform rational design and interpretation of EGFR-targeted therapies in cancer.

Zuo Y, Schwartz HT, Walker K et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Precision Medicine in Pancreatic Cancer: Targeting KRAS and Beyond.

This review article assessed the emerging precision medicine strategy in advanced/metastatic pancreatic cancer focusing on targeting mutant KRAS and related pathways, contextualizing results from the RASolute 302 trial. The key finding was that RAS inhibition demonstrated clinically meaningful activity in metastatic pancreatic cancer, expanding the subset of patients who can receive targeted therapy beyond historically limited options. Scientifically and clinically, it supports KRAS-directed treatment as a new therapeutic foundation and frames future combination and biomarker-driven approaches.

Schürmann H, Park W, O’Kane GM et al. · Targeted oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Abemaciclib rechallenge after progression on abemaciclib plus endocrine therapy in patients with hormone receptor-positive HER2-negative metastatic breast cancer: results from the phase II again study (WJOG14220B).

This phase II multicenter, single-arm again study evaluated abemaciclib rechallenge in hormone receptor-positive, HER2-negative metastatic breast cancer patients who progressed after prior abemaciclib plus endocrine therapy (CDK4/6 inhibitor + ET). The key finding was that continuing abemaciclib while switching endocrine partner (switching from aromatase inhibitor/tamoxifen to fulvestrant or from fulvestrant to AI/TAM) produced a measurable progression-free survival benefit after progression on the prior regimen. Clinically, it suggests that abemaciclib rechallenge with endocrine switching may be a viable option for a post–CDK4/6 inhibitor population with limited subsequent choices.

Nishimura M, Kogawa T, Sugiyama K et al. · Breast cancer research and treatment · (2026) · View on PubMed ↗ · Free PDF ↗

Tailored strategies to overcome third-generation TKI resistance in EGFR-mutated non-small cell lung cancer.

This review article summarized evidence for tailored strategies to overcome third-generation EGFR TKI resistance in EGFR-mutated non-small cell lung cancer, focusing on resistance mechanisms and how they inform treatment selection. It covers acquired resistance including on-target EGFR alterations such as EGFR C797S and other kinase-domain mutations, off-target pathway activation (e.g., MET or HER2 amplification, RAS-MAPK signaling, and oncogenic fusions), and neuroendocrine transformation to small-cell lung cancer. The scientific significance is that it provides a framework for matching specific resistance genotypes/phenotypes to next-line therapeutic strategies to improve outcomes in precision oncology.

Saporita I, Farinea G, Lombardi E et al. · Expert opinion on therapeutic targets · (2026) · View on PubMed ↗

Targeted mRNA Delivery Using Bispecific Antibody-Lipid Nanoparticle Complexes.

This study developed and tested targeted mRNA delivery using bispecific antibody–lipid nanoparticle complexes (TbsAb-LNPs) designed to improve extrahepatic, tissue- and cell-specific uptake beyond conventional lipid nanoparticles. The authors created a bispecific targeting platform that binds LNP polyethylene glycol (PEG) components and used it to model targeted uptake in vitro prior to in vivo application (full experimental outcomes truncated). This platform advances targeted RNA therapeutics by enabling more precise delivery to specific cellular/tissue compartments.

Hickey JC, Roach T, Cassaidy B et al. · Molecular pharmaceutics · (2026) · View on PubMed ↗

Eltrombopag Added to Standard Immunosuppressive Treatment as Front-Line Therapy for Severe Aplastic Anemia: Long-Term Outcomes of the Phase-3 Randomized Superiority EBMT-SAAWP RACE Study.

This phase 3 randomized superiority trial (EBMT-SAAWP RACE; NCT02009747) compared horse antithymocyte globulin (hATG) plus cyclosporine A (CsA) versus the same standard immunosuppressive therapy with added eltrombopag as front-line treatment in 197 treatment-naive patients with severe aplastic anemia. The final 2-year analysis showed a significantly higher 2-year cumulative incidence of complete response with eltrombopag added to standard IST (arm B) than with standard IST alone (arm A). These long-term results strengthen evidence that eltrombopag improves durable hematologic response rates in severe aplastic anemia when used upfront.

Risitano AM, Iacobelli S, Kulasekararaj A et al. · American journal of hematology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Genomics, Proteomics & Multi-omics

Incidence, risk factors and tumor spectrum of second primary cancers after gastric cancer: a multicenter cohort study with long-term follow-up.

This multicenter cohort study evaluated long-term incidence, risk factors, and tumor spectrum of second primary cancers (SPCs) in gastric cancer survivors who underwent curative-intent radical gastrectomy (2007–2021) in the MAGIS cohort. The key findings (from the study’s long-term follow-up design) identify clinical factors associated with SPC occurrence and characterize detection patterns and stage distribution of SPCs over time. These results are significant for guiding SPC surveillance strategies and risk stratification after gastrectomy.

Gao X, Han W, Lu L et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Structures of dynamic interactors at native proteasomes by PhIX-MS and cryo-electron microscopy.

This study developed PhIX-MS (photo-induced in situ crosslinking-mass spectrometry) combined with cryo-electron microscopy to capture dynamic, transient interactions at native proteasomes. Using this workflow, the authors mapped the redox sensor TXNL1 at the proteasome regulatory particle (RP), including its dynamic thioredoxin-like domain near RPN2/PSMD1 and RPN13/ADRM1, and resolved RP structures bound to TXNL1 even without the proteolytic core particle. Scientifically, the approach clarifies how transient redox interactions are organized at the proteasome to support substrate reduction prior to proteolysis.

Lee K, Negi H, Chen X et al. · Molecular cell · (2026) · View on PubMed ↗

Multiomics integrative bioinformatics analysis of gene expression characteristics and molecular mechanisms in preeclampsia placental tissue.

This integrative multiomics bioinformatics study analyzed preeclampsia placental tissue by combining multiple placental transcriptome datasets and single-cell sequencing data from GEO using differential expression, WGCNA, and machine-learning approaches to define molecular mechanisms and subtypes. The analysis identified gene expression characteristics and co-expression modules associated with preeclampsia and proposed molecular subtypes and pathways underlying placental dysfunction. Clinically, such subtype- and pathway-level insights could support improved biomarker discovery and more mechanism-driven stratification of preeclampsia.

Li N, Tian L, Wei H · Artificial cells, nanomedicine, and biotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Temporal variability in outcomes of identical regimens across newly diagnosed myeloma trials: a systematic review.

This systematic review assessed how progression-free survival (PFS) outcomes for identical myeloma regimens vary across newly diagnosed myeloma trials, focusing on VRd (bortezomib/lenalidomide/dexamethasone) or Rd (lenalidomide/dexamethasone) without transplant. The authors analyzed factors that could contribute to temporal variability in PFS, including informative censoring and diagnostic changes affecting inclusion of patients previously classified as smoldering myeloma (full results truncated). Understanding these sources of outcome drift improves the validity of cross-trial comparisons and supports more accurate interpretation of regimen efficacy over time.

Mohyuddin GR, Vaquera-Alfaro HA, Godara A et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Redefining functional high-risk multiple myeloma in the context of upfront quadruplet therapy and autologous stem cell transplantation.

This analysis studied how to redefine functional high-risk (FHR) multiple myeloma in the era of upfront quadruplet therapy plus autologous stem cell transplantation (QUAD + ASCT) by analyzing 310 newly diagnosed MM patients. The authors evaluated progression-based cutoff definitions for FHR and examined factors associated with outcomes of subsequent therapy (specific optimal cutoff and results are truncated). A revised FHR definition tailored to modern QUAD + ASCT regimens can better stratify patients and guide treatment decisions.

Ravi G, Dhakal B, Callander NS et al. · Cancer · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Pan-cancer proteogenomic interrogation of the ubiquitin-proteasome system.

This study used harmonized pan-cancer proteogenomic data from up to 11 CPTAC cohorts to interrogate how somatic cancer-driver alterations remodel the ubiquitin-proteasome system (UPS) at the protein level, focusing on UPS protein dysregulation, prognostic associations, and mutation-driven remodeling. It found that mRNA poorly predicts UPS protein abundance, that a recurrent set of E3 ligases is dysregulated across cancers, and that somatic mutations—most notably TP53 loss—produce coherent UPS protein quantitative trait locus (pQTL) signatures. These findings support mutation-informed UPS targeting by showing that proteome-level UPS remodeling is a key determinant of tumor biology and potential therapeutic response beyond transcriptomics.

González-Robles TJ, Khan M, Sastourné P et al. · Cell death and differentiation · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.

This review synthesized current knowledge on tumor evolution, emphasizing signaling pathways, molecular mechanisms, and therapeutic targets, and how modern technologies enable dynamic characterization of evolutionary trajectories. The key finding is that high-throughput sequencing, single-cell and spatial omics, lineage tracing, computational modeling, and noninvasive biopsy approaches collectively improve understanding of heterogeneity and adaptation in advanced cancer. The significance is that it supports evolution-informed therapeutic targeting by connecting evolutionary dynamics to potential intervention points.

Zhang KY, Zhu XZ, Yan YX et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

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Epitranscriptomics & RNA Regulation

Promoter strength and position govern promoter competition through transcript-dependent insulation.

This study examined how promoter strength and genomic position determine promoter competition at the Sox2 locus by inserting diverse promoters into defined genomic sites and measuring effects on endogenous Sox2 transcription. It found that the reduction in endogenous Sox2 expression correlates with inserted promoter strength, that competition requires transcription from the inserted promoter, and that longer transcripts produce more competition via transcript-dependent insulation. This is significant for understanding how regulatory architecture and transcriptional output govern enhancer/promoter competition in development and disease.

Koska M, Nagano M, Swigut T et al. · Nature genetics · (2026) · View on PubMed ↗

A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death.

This study created a small-molecule chemically induced proximity (CIP) strategy using lysine acetyltransferase (KAT)-based TCIPs (KAT-TCIPs) to induce oncogene-induced cell death in diffuse large B cell lymphoma (DLBCL). By redirecting p300/CBP to activate cell-death networks repressed by the oncogenic driver BCL6, the lead KAT-TCIP reprogrammed the epigenome and initiated apoptosis. The mechanistic significance is that KAT-TCIPs provide a targeted, proximity-based way to kill BCL6-driven lymphoma cells and potentially prevent relapse.

Nix MN, Gourisankar S, Bowman KJ et al. · Cell · (2026) · View on PubMed ↗

RNA exonuclease REXO4 resolves m6A-marked R-loops and suppresses anti-tumor immunity.

This study investigated how the RNA exonuclease REXO4 regulates R-loop homeostasis in human cells and its impact on anti-tumor immunity. It found that REXO4 resolves m6A-marked R-loops by 3’-5’ exonucleolytic cleavage of the RNA strand within RNA-DNA hybrids, with m6A promoting REXO4 localization and R-loop removal. The significance is that loss of REXO4 increases DNA damage and triggers interferon responses with tumor immune infiltration, suggesting REXO4 as a potential target to modulate anti-tumor immunity.

Zhang J, Bao K, Hou Y et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

A genome-wide functional analysis of conserved intronic regions reveals essential roles for speckle-associated retained introns.

This genome-wide functional study used a dual CRISPR-Cas editing strategy to delete 2,600 conserved human intronic regions associated with intron retention, focusing on speckle-associated retained introns in human cells. The key finding was that a subset of these conserved “fitness” intronic sequences affects cell growth by altering intron retention and host gene expression, with deletions in nuclear speckle-associated retained introns in FNBP4 and DDX5 producing downstream effects. These results establish conserved retained introns as functional regulatory elements essential for RNA processing and gene expression programs.

Farhangmehr S, Braunschweig U, Wu M et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

RNA modifications in cancer: regulators of tumor evolution and therapeutic response.

This review examined how RNA modifications—such as m6A, m1A, m5C, m7G, pseudouridine (Ψ), and A-to-I editing—regulate tumor evolution and therapeutic response through the epitranscriptomic network of writers, readers, and erasers. The key finding is that dysregulated RNA modification machinery can control transcript stability and translation efficiency, thereby shaping cancer progression and treatment sensitivity. Scientifically, it consolidates mechanistic links between epitranscriptomic regulation and actionable therapeutic opportunities across cancer types.

Gu X, He Y, Xu Z et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Tumor Microenvironment & Response Biomarkers

Single-Cell Analysis of Residual Esophageal Squamous Cell Carcinoma After Neoadjuvant Immunochemotherapy Reveals TFAM-Mediated Immunoregulation in Dendritic Cells.

This study performed single-cell analysis of tumor microenvironments in 14 patients with esophageal squamous cell carcinoma (ESCC) receiving neoadjuvant immunochemotherapy (nICT) to identify cellular programs associated with treatment response. Using nonnegative matrix factorization (NMF), it found immunoregulatory programs enriched for immunosuppressive dendritic cell features, with TFAM-mediated immunoregulation in dendritic cells associated with differential pathological tumor regression. These findings suggest TFAM-driven dendritic cell immunoregulation as a mechanistic biomarker and potential target to improve nICT responsiveness in ESCC.

Chen L, Feng T, Zhou J et al. · Cancer research · (2026) · View on PubMed ↗

Immune checkpoint profiling of B7-H proteins predicts survival and treatment response in metastatic clear cell renal cell carcinoma.

This retrospective cohort study profiled immune checkpoint B7-H family proteins (B7-H3, B7-H4, B7-H5, B7-H7) in primary tumor specimens from 145 patients with metastatic clear cell renal cell carcinoma (ccRCC) to determine prognostic and predictive value. Using immunohistochemistry, the authors found marked intratumoral heterogeneity with compartmentalized expression patterns (e.g., B7-H3 in tumor and stroma) and assessed associations with aggressiveness, treatment response, and long-term survival (full associations truncated). If validated, B7-H expression patterns could help predict survival and treatment response in metastatic ccRCC and guide immunotherapy stratification.

Emaldi M, Rey-Iborra E, Mosteiro L et al. · The journal of pathology. Clinical research · (2026) · View on PubMed ↗ · Free PDF ↗

Anatomical and Histologic Response to Neoadjuvant Therapy: Recurrence Patterns Among Poor Responders. A Multi-institutional Observational Cohort Study.

This multi-institutional observational cohort study evaluated how anatomical response to neoadjuvant therapy (NAT), quantified by the Tumor Burden Score ratio (TBSr), and histologic response, assessed by Tumor Regression Grade (TRG), predict recurrence patterns after hepatectomy for colorectal liver metastases (CRLM). It reported that combining TBSr-based macroscopic response with TRG-based histologic response improves characterization of recurrence patterns among poor responders. Clinically, this integrated response assessment could refine post-hepatectomy risk stratification and guide follow-up or additional treatment strategies for CRLM patients after NAT.

Baldo A, Akabane M, Elemosho A et al. · Annals of surgery · (2026) · View on PubMed ↗

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Neurodegeneration & Alzheimer’s/Dementia Biomarkers

Plasma proteome profiling identified biomarkers for the differential diagnosis and molecular staging of neurodegenerative dementias.

Large-scale plasma proteomics was used to profile 1,318 samples from international cohorts to identify blood-based biomarkers for differential diagnosis and molecular staging across Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). More than 200 proteins were dysregulated across disease groups, with glial fibrillary acidic protein (GFAP) most strongly increased along the AD continuum and integrin alpha-V and integrin alpha-M consistently reduced. This provides clinically actionable, scalable protein signatures that may enable improved dementia subtype discrimination and staging.

Bellomo G, Vermunt L, In ‘t Veld S et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

Use of blood-based neurofilament light chain as an endpoint in clinical trials of neurodegenerative conditions: a scoping review.

This scoping review examined interventional neurodegenerative clinical trials (2013–2024) that used blood-based neurofilament light chain (serum or plasma NfL) as an endpoint. The key finding was that blood NfL is increasingly used as a biomarker of neuroaxonal injury, with trial designs and analytical approaches varying across studies, but with consistent support for its feasibility as an outcome measure. Scientifically, the review highlights how blood NfL could standardize and accelerate endpoint selection in neurodegeneration trials.

Zheng Y, Bhalala OG, Chin KS et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Soluble high-molecular-weight amyloid-β species derived from amyloid-β-laden brains induce cerebral β-amyloidosis.

This study investigated whether soluble high-molecular-weight amyloid-β (Aβ) species (>150 kDa) isolated from amyloid-β-laden brains can act as aggregation seeds to initiate and accelerate cerebral β-amyloidosis. Intrahippocampal injection of these soluble >150 kDa Aβ species from plaque-laden APP transgenic mice or Alzheimer’s disease patient brains dramatically accelerated β-amyloidosis in transgenic mouse brains compared with controls. The results identify a specific Aβ strain property (soluble >150 kDa species) that can drive in vivo spreading, advancing understanding of Alzheimer’s disease propagation mechanisms.

Kashiwagi-Hakozaki M, Uchigami H, Naka Y et al. · Brain communications · (2026) · View on PubMed ↗ · Free PDF ↗

Distribution of Big Tau Isoforms in the Human Central and Peripheral Nervous System.

This study mapped the distribution of “big tau” isoforms (tau containing exon 4a) across the human central and peripheral nervous system using mass spectrometry–based sequencing. It found that big tau composition varies anatomically and is present in both CNS and PNS regions, and it assessed disease relevance using postmortem tissues from Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and controls. Scientifically, defining big tau isoform distribution and disease-associated patterns may clarify why peripheral tau biology differs from canonical brain tau and could inform biomarker or mechanism studies in neurodegeneration.

Koppisetti RK, Barthélemy NR, Horie K et al. · Annals of neurology · (2026) · View on PubMed ↗

Blood-based multimodal biomarker models for differentiating early-onset Alzheimer’s disease from frontotemporal dementia: a longitudinal study of early-onset dementia and family members (LEAF) study.

This longitudinal LEAF study analyzed blood-based multimodal biomarker models to differentiate early-onset Alzheimer’s disease (EOAD) from early-onset frontotemporal dementia (EOFTD) in 185 participants (EOAD n=150, EOFTD n=35, age ≤65) using plasma immunoassays for p-tau217, p-tau181, neurofilament light (NfL), and GFAP. Plasma p-tau217 and p-tau181 showed high discriminative performance (AUC 0.831 and 0.862, respectively) for distinguishing EOAD from EOFTD. These results extend the diagnostic utility of plasma phosphorylated tau biomarkers to early-onset populations and support blood-based differential diagnosis models for clinical use.

Kwon HS, Moon SY, Hwang M et al. · Journal of neurology · (2026) · View on PubMed ↗

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Neuroinflammation, Microglia & CNS Immunity

Microglial states revisited: from homeostasis to disease.

This review studied microglial state diversity across development, brain region, sex, age, genotype, and environment, focusing on how modern multi-omics approaches reshape microglial classification. It found that single-cell/single-nucleus transcriptomics, chromatin accessibility profiling, and spatial multi-omics support a multidimensional microglial state space rather than binary “resting vs activated” or M1/M2 frameworks. Scientifically, this reframes how microglial “homeostatic” and “disease-associated” signatures are interpreted in brain development and neurodegeneration.

Eggen BJL, Kooistra SM · Nature reviews. Neuroscience · (2026) · View on PubMed ↗

Complement dysregulation during the early phases of synucleinopathy.

This study investigated complement dysregulation during early synucleinopathy using a rat α-syn preclinical model to test whether complement activation is driven directly by pathological α-syn versus occurring only after overt neurodegeneration. The key finding is that complement cascade activation occurs during early phases of synucleinopathy, supporting a more direct link between α-syn pathology and neuroinflammatory mechanisms. This is significant for identifying complement as a potential early therapeutic target in Parkinson’s disease and related synucleinopathies.

Khan H, Gifford M, Kordbacheh A et al. · Acta neuropathologica · (2026) · View on PubMed ↗ · Free PDF ↗

The orchestration of ciliary opus: Interplay of signalling molecules, GTPases, and trafficking machinery.

This Current Opinion review summarized how primary cilia signaling is orchestrated by the interplay of intraflagellar transport (IFT) machinery, the BBSome coat complex, small GTPases, and trafficking regulators. It highlights that kinesin-2 and dynein-2 motors coordinate bidirectional receptor and signaling-component trafficking, while ciliary lipid composition and secondary messengers such as cAMP and Ca2+ regulate ciliary composition and signaling. The significance is a systems-level framework for understanding how ciliary trafficking and signaling integration maintain tissue homeostasis and how dysregulation can drive disease.

Piyush R, Giri P, Shinde SR · Current opinion in cell biology · (2026) · View on PubMed ↗

Unlocking Sulforaphane’s Potential in Friedreich Ataxia: Further Evidence from Preclinical Investigations Using Induced Pluripotent Stem Cell-Derived Sensory Neurons.

This preclinical study compared sulforaphane (SF) with the approved Friedreich ataxia therapy omaveloxolone (Omav) and with dimethyl fumarate (DMF) in induced pluripotent stem cell (iPSC)-derived sensory neurons from Friedreich ataxia patients carrying expanded GAA repeats in the FXN gene (including a line with 550 GAA1 repeats). The key finding was that SF further supported FXN upregulation and beneficial modulation of epigenetic, inflammatory, and oxidative stress pathways in these patient-derived neurons, aligning with or extending prior observations. The clinical significance is that SF emerges as a promising therapeutic candidate for FRDA alongside (and potentially in comparison with) Omav and DMF, warranting further translational development.

Yang W, Thompson B, Miellet S et al. · Antioxidants & redox signaling · (2026) · View on PubMed ↗

Small Extracellular Vesicles From Cardiomyocytes Activate Microglia Aggravating HFpEF.

The study investigated whether small extracellular vesicles (sEVs) released from cardiomyocytes activate hypothalamic microglia and worsen heart failure with preserved ejection fraction (HFpEF) using a mouse model combining long-term high-fat diet and the nitric oxide synthase inhibitor L-NAME. In HFpEF mice, microglial activation and hypothalamic inflammation were observed, and microglial depletion with PLX3397 suppressed downstream sympathetic activation, implicating cardiomyocyte-derived sEV signaling in HFpEF neuroinflammation. These findings support sEV–microglia crosstalk as a mechanistic target for therapies aimed at neuroinflammation and sympathetic overactivity in HFpEF.

Men L, Wang Q, Ren B et al. · Circulation research · (2026) · View on PubMed ↗

Gut microbiota-driven metabolites modulate the development of stress-related mental disorders.

This review synthesized evidence on how gut microbiota-driven metabolites influence the development of stress-related mental disorders, including depression, anxiety, and post-traumatic stress disorder. The key finding is that microbiota alterations can change metabolite production and systemic exposure, thereby modulating host physiology relevant to stress-pathology. Scientifically, it frames gut-microbiome metabolite pathways as actionable mechanistic links and potential therapeutic targets for stress-related psychiatric conditions.

Yuan M, Qin F, Wu L et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious Disease (Antivirals, Vaccines, Host-Directed Therapies)

Circulating alpha-1 antitrypsin and its c-terminal peptides differentiate bacterial from viral community-acquired pneumonia.

Researchers studied whether circulating alpha-1 antitrypsin (AAT) and nine AAT-derived C-terminal peptides can distinguish bacterial from viral community-acquired pneumonia in 81 prospectively enrolled adults at hospital admission (day 0) and day 3. Using ELISA for AAT and LC-based peptide quantification, they found that AAT/peptide profiles differentiate bacterial versus viral CAP. This is clinically significant because it could reduce inappropriate antimicrobial use by improving early CAP etiologic classification.

Pashai Fakhri M, Börner FR, Held J et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Viral syncytia evolve to resist interferon.

This study examined how SARS-CoV-2 spike (S)-mediated viral syncytia formation affects interferon responses and antibody neutralization, using SARS-CoV-2 and spike-replacement vesicular stomatitis virus (VSV) in cultured cells, human lung cell cultures, and hACE2 transgenic mice. It found that S-driven syncytia impair interferon antiviral effects and that spike amino-acid substitutions that modulate syncytia formation confer parallel interferon resistance in Delta and Omicron. This is significant because it links a viral cell-fusion phenotype to immune evasion and may inform antiviral or vaccine strategies targeting spike-mediated entry/fusion.

Li T, Kang I, Ye J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Mapping in-cell protein contact sites reveals hijacking of paraspeckles during influenza A virus infection.

In human cells infected with influenza A virus (IAV), the authors used in-cell cross-linking mass spectrometry combined with structural modelling and functional assays to map native-context virus–host protein contact sites. They uncovered previously unrecognized interactions, including host factors in the membrane-bound endoplasmic reticulum–Golgi system that regulate maturation of distinct haemagglutinin (HA) glycoforms. This mechanistic map of in-cell contact sites clarifies how IAV hijacks spatially organized host processes and can guide antiviral target discovery.

Kotova I, Mühlberg L, Gilep K et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

All-trans retinoic acid suppresses systemic inflammation induced by severe fever with thrombocytopenia syndrome virus in mice.

The study examined whether all-trans retinoic acid (ATRA) modulates systemic inflammation during severe fever with thrombocytopenia syndrome virus (SFTSV) infection in patients and in an SFTSV mouse model. In patients, serum vitamin A/ATRA were depleted and this correlated with worse systemic inflammatory response syndrome severity and mortality, while in mice intraperitoneal ATRA suppressed virus-induced hyperinflammation via PPARγ-dependent downregulation of macrophage AP-1 transcriptional activity. These results support ATRA as a potential host-directed anti-inflammatory therapy for SFTSV.

Yu X, Wu J, Yin X et al. · Nature microbiology · (2026) · View on PubMed ↗

Effect of high-dose versus standard-dose influenza vaccines on hospitalisation outcomes and mortality in older adults: a systematic review and meta-analysis.

This systematic review and meta-analysis compared high-dose inactivated influenza vaccine (HD-IIV; 60 μg haemagglutinin per strain) versus standard-dose inactivated influenza vaccine (SD-IIV) in adults aged 65 years or older using randomized controlled trials. The key finding was that HD-IIV provides improved protection against clinically important outcomes, including influenza-related hospitalisation and mortality, relative to SD-IIV in older adults. This supports preferential use of HD-IIV in geriatric immunization strategies to reduce severe influenza burden.

Zhao W, Lian R, Zhao Y et al. · The lancet. Healthy longevity · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Viral protease-initiated lytic cell death as a universal antiviral mRNA therapy.

This preclinical study developed viral protease-initiated lytic cell death (VID), a universal mRNA therapeutic platform, by engineering gasdermin-D (GSDMD) with viral protease-specific cleavage motifs to create VID activators (VIDAs). In a hepatitis A virus (HAV) model delivered as lipid nanoparticle (LNP)-encapsulated VIDA mRNA, VIDAs selectively triggered lytic cell death in virus-infected cells, abolished viral replication and shedding in vivo, and mitigated liver injury. The work suggests a broadly applicable antiviral mRNA strategy that converts viral protease activity into an intracellular “kill” signal to limit infection and tissue damage.

Li L, Yan XL, Wang HY et al. · Cell · (2026) · View on PubMed ↗

Clesrovimab in Infants at Increased Risk For Severe Disease During 2 RSV Seasons: A Randomized Clinical Trial.

This randomized clinical trial evaluated clesrovimab, a long-acting monoclonal antibody, in infants at increased risk for severe respiratory syncytial virus (RSV) disease across two RSV seasons, comparing clesrovimab (105 mg) with palivizumab in season 1 and assessing safety of 210 mg clesrovimab in season 2. The key finding was that clesrovimab had an acceptable safety and tolerability profile in this high-risk infant population across the two seasons. Clinically, it supports the use of clesrovimab as an alternative to palivizumab for RSV prevention in infants who remain at risk beyond the first season.

Zar HJ, Bont LJ, Manzoni P et al. · JAMA pediatrics · (2026) · View on PubMed ↗ · Free PDF ↗

Divergent Autophagy Pathways in Plasmodium: Mechanisms, Functions, and Therapeutic Potential.

This review examined autophagy in the malaria parasite Plasmodium, focusing on the reduced but functional autophagy-related (ATG) protein repertoire and the role of ATG8 in parasite cells. It found that Plasmodial autophagy is organized through divergent, branched ATG8 localization that associates with the relict plastid (apicoplast) membrane, implying functions beyond canonical autophagy. These parasite-specific autophagy mechanisms highlight ATG8 and related pathways as potential therapeutic targets for malaria by exploiting differences from yeast/mammalian autophagy.

Rajput S, Mehra P, Nandi R et al. · Molecular microbiology · (2026) · View on PubMed ↗

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Respiratory Medicine (Asthma/COPD/ARDS/ENT)

Phase III LUNA clinical programme: design of four randomised, double-blind, placebo-controlled studies assessing the efficacy and safety of tozorakimab in patients with symptomatic COPD and a high risk of exacerbations.

The LUNA programme was designed as four multicentre, randomized, double-blind, placebo-controlled phase III studies to test tozorakimab, an anti-IL-33 monoclonal antibody that inhibits both IL-33red and IL-33ox, in symptomatic COPD patients with a high risk of exacerbations. The trials enroll participants receiving optimized inhaled therapy and evaluate efficacy and safety across ongoing studies including OBERON (NCT05166889) and TITANIA (NCT05158387). This programme targets IL-33 biology to reduce COPD exacerbations and inform late-stage clinical benefit.

Watz H, Sciurba FC, Bonini M et al. · BMJ open respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗

Use of tezepelumab for chronic rhinosinusitis with nasal polyps by eosinophilic endotype: WAYPOINT post-hoc analysis.

This post-hoc analysis of the phase 3 WAYPOINT trial (NCT04851964) evaluated tezepelumab 210 mg versus placebo every 4 weeks in Japanese adults with severe chronic rhinosinusitis with nasal polyps (CRSwNP), stratified by eosinophilic chronic rhinosinusitis defined by the Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis (ECRS). Tezepelumab improved nasal polyp outcomes and sinonasal symptoms and showed a safety profile consistent with prior results across eosinophilic ECRS subgroups. Clinically, the data support using tezepelumab for CRSwNP patients with an eosinophilic endotype, potentially reducing reliance on systemic corticosteroids and surgery.

Fujieda S, Otori N, Han JK et al. · Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Prone positioning in ARDS.

This narrative review summarized the evidence and clinical role of prone positioning in acute respiratory distress syndrome (ARDS), including early use in intubated patients with PaO2/FiO2 <150 mmHg and the awake prone position (APP) approach used more broadly after COVID-19. The key finding was that prone positioning reliably improves oxygenation in both intubated and non-intubated settings, while the optimal implementation in routine non-COVID ICU practice still requires further confirmation. The clinical significance is that prone positioning remains a lung-protective strategy, with ongoing refinement needed for patient selection and timing.

Ehrmann S, Li J, Liu L et al. · Intensive care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

The Airway Transcriptome in Type 2 Cytokine Biomarker-High and -Low Severe Asthma.

This study characterized the airway transcriptome in severe asthma stratified by type 2 (T2) cytokine biomarker status using bronchial biopsies and brushes from the UK Refractory Asthma Stratification Programme cohort. By comparing T2 biomarker-high (n=18), T2-intermediate (n=23), and T2-low (n=11) groups plus healthy controls (n=20) before and after high-dose inhaled corticosteroids, the authors identified dysregulated genes and pathways that differ by T2 biomarker level. The clinical significance is improved mechanistic understanding of T2-low severe asthma, which may guide development of targeted therapies beyond corticosteroid-responsive T2 inflammation.

Shen J, Chaudhuri R, Bicknell S et al. · Allergy · (2026) · View on PubMed ↗ · Free PDF ↗

Ruxolitinib cream in adults with moderate atopic dermatitis after failure of other topicals: A randomized trial.

This randomized trial studied ruxolitinib cream in adults (≥18 years) with moderate atopic dermatitis (IGA 3, EASI >7, itch NRS ≥4) who had inadequate response, intolerance, or contraindications to topical corticosteroids (TCS) and topical calcineurin inhibitors (TCI) within the prior 12 months in the TRuE-AD4 study (NCT06238817). Ruxolitinib cream produced clinically meaningful improvements by 8 weeks in disease signs/symptoms and itch compared with the trial’s control regimen (details truncated in the abstract). These findings support ruxolitinib cream as a targeted topical JAK inhibitor option for adults with moderate AD who fail standard topical anti-inflammatory therapies.

Carrascosa JM, Prajapati VH, Hong HC et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗ · Free PDF ↗

Cigarette Smoke-Exposed Alveolar Epithelial Cell-Derived Exosomes Exacerbate Skeletal Muscle Dysfunction Through HDAC2 Signalling.

This study investigated whether exosomes derived from cigarette smoke–exposed alveolar epithelial cells drive skeletal muscle dysfunction in the context of COPD, with emphasis on histone deacetylase 2 (HDAC2) signaling. Using the exosome inhibitor GW4869 in a chronic cigarette smoke exposure model, it found that these exosomes exacerbate skeletal muscle dysfunction by regulating HDAC2-dependent inflammatory transcriptional control. The findings support a mechanistic exosome–HDAC2 axis linking lung injury to systemic sarcopenia-like muscle impairment, suggesting potential targets to mitigate COPD-related skeletal muscle dysfunction.

Li C, Ou M, Jiang G et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular Disease & Vascular Biology

Does Characterization of Phenotypic Heterogeneity Provide Mechanistic Insights or Influence the Response to Treatment? Experience in Positive and Neutral Trials in Patients With Heart Failure and a Preserved Ejection Fraction.

This article reviewed and analyzed whether characterizing phenotypic heterogeneity in heart failure with preserved ejection fraction (HFpEF) can yield mechanistic insights or identify treatment responders, drawing on experience from positive and neutral HFpEF trials. The key finding was that subgroup analyses based on phenotypic diversity have not reliably identified responders or translated into broadly effective, mechanism-driven therapies. Scientifically, it argues for more rigorous, hypothesis-driven stratification approaches beyond descriptive phenotyping in HFpEF.

Packer M, Schiattarella GG, Petrie MC et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗

Loss of ATP-Dependent Citrate Lyase Drives Left Ventricular Dysfunction by Metabolic Remodeling.

This study investigated how loss of ATP-dependent citrate lyase (ACL/ACLY) affects cardiac metabolism and function by using human heart tissue from healthy donors and patients with nonischemic cardiomyopathy and applying CRISPR-based approaches to perturb ACL. The key finding was that ACL loss drives left ventricular dysfunction through metabolic remodeling, consistent with impaired acetyl-CoA production and downstream lipid synthesis programs. Clinically, it highlights ACL as a metabolic vulnerability and potential therapeutic target in nonischemic cardiomyopathy and heart failure.

Liu S, Gammon ST, Tan L et al. · Circulation · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Implications of the 2026 Dyslipidemia Guideline for Primary Prevention Statin Therapy.

This study assessed the population health impact of the 2026 American Heart Association/American College of Cardiology/multisociety dyslipidemia guideline on primary prevention statin eligibility among nonpregnant adults aged 30–79 years without known ASCVD using NHANES 2017–2023 data. The key finding was that the guideline’s updated ASCVD risk estimation and expanded statin-eligible populations would substantially increase the proportion of adults recommended for primary prevention statin therapy. These results suggest the 2026 guideline could meaningfully shift real-world statin use and downstream cardiovascular risk reduction at the population level.

Anderson TS, Wilson LM, Sussman JB · JAMA · (2026) · View on PubMed ↗ · Free PDF ↗

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Critical Care & Perioperative Medicine

Mitochondrial-derived vesicles drive budding-type fission of damaged lysosomes.

Researchers studied lysosomal renewal under hypoxia-reoxygenation stress by identifying a budding-type fission (B-fission) pathway that restores lysosomal function independently of autophagic lysosome reformation. They found that damaged lysosomes generate membrane buds that undergo scission to form small functional lysosomes, and that mitochondrial-derived vesicles (MDVs) deliver the fission adaptor MFF to lysosomes to recruit DRP1. This is significant because it reveals a new organelle-maintenance mechanism that could be targeted to preserve lysosomal function during stress.

Luo Y, Yu J, Li Z et al. · Nature cell biology · (2026) · 1 citations · View on PubMed ↗

Patient-reported Outcomes After Prostate Stereotactic Body Radiotherapy at 5 yr: Results from the PACE-B Trial.

In the phase 3, international PACE-B trial, patient-reported outcomes were assessed at 5 years in men with localized prostate cancer randomized to stereotactic body radiotherapy (SBRT) versus conventionally fractionated radiotherapy (CRT). At 5 years, urinary incontinence outcomes were favourable and comparable between SBRT and CRT, with leak-free rates reported as 64% (164/…). These long-term PROM data support patient-centered decision-making when choosing between SBRT and CRT for localized prostate cancer.

Cooper S, Patel J, Moore C et al. · European urology · (2026) · View on PubMed ↗ · Free PDF ↗

COVID-19 and Global Perinatal Health: Lessons Learned on Maternal-Neonatal Outcomes, Infant Feeding Practices, and Healthcare Economics Across Income Settings.

This narrative review synthesized global evidence on how the COVID-19 pandemic affected maternal-neonatal outcomes, infant feeding practices, and healthcare economics across high-income countries (HICs) and low- and middle-income countries (LMICs). The review concludes that both direct SARS-CoV-2 infection and indirect healthcare-system disruption were associated with worse perinatal outcomes, altered breastfeeding practices, and substantial financial burden on healthcare institutions, with impacts differing by income setting. These cross-setting findings highlight where maternal-newborn care and breastfeeding support need strengthening during ongoing or future health-system shocks.

Gunasekaran V, Woo S, Shetty AK et al. · American journal of perinatology · (2026) · View on PubMed ↗

Global, regional, and national burden of road injuries 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023.

This Global Burden of Disease Study 2023 analysis estimated the global, regional, and national incidence, mortality, and morbidity of road injuries across 204 countries and territories from 1990 to 2023. The study found substantial and persistent geographic variation in road-injury burden over time, providing updated metrics to track progress toward the UN Decade of Action for Road Safety targets. Public-health significance lies in identifying where intervention gaps remain most urgent for reducing road traffic deaths and serious injuries.

The Lancet. Public health · (2026) · View on PubMed ↗ · Free PDF ↗

Immune-Enhancing Nutrition and Outcomes After Radical Cystectomy: A Randomized Clinical Trial.

This multicenter, randomized, double-blind phase 3 trial (SWOG S1600) studied whether perioperative specialized immunonutrition reduces 30-day complications compared with standard oral nutrition support in adults undergoing radical cystectomy for bladder cancer. The key finding was that immune-enhancing nutrition improved postoperative outcomes by lowering early complication rates relative to standard nutrition support. Clinically, it supports incorporating targeted immunonutrition into perioperative care to reduce morbidity after radical cystectomy.

Hamilton-Reeves JM, Unger JM, Holzbeierlein JM et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists and All-Cause Overdose Risk in Veterans With Type 2 Diabetes and Opioid Use Disorder.

This target trial emulation study used Veterans Health Administration data to compare overdose risk among Veterans with type 2 diabetes and opioid use disorder who initiated semaglutide or tirzepatide versus initiation of other diabetes medications (e.g., insulin, metformin, sulfonylurea, SGLT2 inhibitor). The key finding was that GLP-1 receptor agonist initiation was associated with a lower all-cause overdose risk compared with the diabetes medication comparator group. Clinically, it supports the potential of GLP-1RAs as an adjunct strategy to reduce overdose harm in a high-risk OUD population.

Kennedy KP, Bremseth-Vining R, Lynch KG et al. · The Journal of clinical psychiatry · (2026) · View on PubMed ↗

PROSPECT guideline for total hip arthroplasty: updated systematic review and procedure-specific postoperative pain management recommendations.

This PROSPECT collaboration updated systematic review evaluated randomized trials and systematic reviews (Jan 2020–Jun 2024) to produce procedure-specific postoperative pain management recommendations for elective primary total hip arthroplasty. The update specifically incorporates new evidence on motor-sparing regional techniques and revises the 2021 PROSPECT recommendations for analgesic efficacy, safety, and functional recovery. Clinically, it aims to standardize peri-operative pain strategies to improve postoperative outcomes while minimizing adverse effects after total hip arthroplasty.

Carella M, Bugada D, Van de Velde M et al. · Anaesthesia · (2026) · View on PubMed ↗ · Free PDF ↗

Sustainable miniaturized smartphone-coupled TLC platform for innovative cleaning validation: application to tizanidine combinations under challenging concentration ratios.

This work developed a sustainable, miniaturized smartphone-coupled thin-layer chromatography (TLC) platform to support pharmaceutical cleaning validation for tizanidine (TZN) carryover under challenging concentration ratios in combination with aceclofenac (ACF), ibuprofen (IBF), and paracetamol (PRC). The key finding is that the at-line portable TLC approach enables rapid determination of TZN in multi-drug mixtures to address cross-contamination risk from narrow-therapeutic-index, high-abuse-potential drugs. Clinically and operationally, the method offers a practical monitoring tool to improve routine cleaning validation and reduce patient-safety risks from drug carryover.

Abd El-Aziz MO, Nadim AH, Monir HH et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Hemoperfusion during extracorporeal membrane oxygenation: an updated systematic review and meta-analysis of 8,151 patients.

This systematic review and meta-analysis evaluated clinical efficacy and safety of hemoperfusion (HP) added to extracorporeal membrane oxygenation (ECMO) versus ECMO alone in adults, pooling 8,151 patients across studies. The key finding is the comparative assessment of all-cause mortality as the primary outcome, with subgroup analyses by study design (RCT vs non-RCT), ECMO type (VA vs VV), and etiology (cardiogenic shock vs cardiac arrest). Clinically, it aims to clarify whether ECMO+HP improves survival and safety in critically ill adult populations where extracorporeal support is used.

Xie T, Yang C, Tao H et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Sodium bicarbonate therapy in severe metabolic acidemia: an individual patient data meta-analysis of the BICAR-ICU and BICAR-ICU2 trials.

This individual patient data meta-analysis combined the BICAR-ICU and BICAR-ICU2 randomized trials to test intravenous sodium bicarbonate therapy in adults with severe metabolic acidemia (pH ≤ 7.20), comparing bicarbonate titrated to pH ≥ 7.30 versus no bicarbonate. The key finding is the pooled estimate of effects on 90-day mortality and renal replacement therapy (RRT) use, including exploration of heterogeneity across prespecified subgroups. The clinical significance is that it provides higher-resolution evidence to guide bicarbonate use in severe metabolic acidemia and to identify patient groups most likely to benefit or be harmed.

Fosset M, Pensier J, Jabaudon M et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Lyophilized platelet derived extracellular vesicles promote hemostasis and attenuate intracranial hemorrhage following traumatic brain injury.

This study evaluated whether lyophilized platelet-derived extracellular vesicles (LPEVs) improve hemostasis and reduce intracranial hemorrhage (ICH) after traumatic brain injury (TBI) in a murine TBI model, with characterization by flow cytometry, scanning electron microscopy, and Nanosight and functional testing on human brain endothelial cell monolayers. LPEV treatment preserved blood–brain barrier integrity and attenuated ICH compared with controls. The results support LPEVs as a translational, cell-derived therapeutic strategy to mitigate TBI-associated bleeding and vascular dysfunction.

Trivedi A, Miyazawa B, Fields AT et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Diabetes, Obesity & Metabolic Health

EndoBridge 2025: pearls and highlights.

EndoBridge 2025 was studied as a scientific meeting (Antalya, Türkiye, Oct 23–26, 2025) covering major topics in endocrinology and metabolism, including pituitary, thyroid, adrenal, bone metabolism, neuroendocrine tumors, diabetes, obesity, nutrition, and lipid disorders. The key finding is that the congress delivered state-of-the-art lectures and interactive case discussions with broad international participation and coverage of current clinical and research directions. This is significant as a platform for disseminating emerging endocrinology knowledge and shaping clinical practice discussions.

Yildiz BO, Armenti M, Brandi ML et al. · Hormones (Athens, Greece) · (2026) · View on PubMed ↗

Effects of Lifestyle Modification on Intrapancreatic Fat Deposition: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated whether lifestyle modification interventions (across included studies) reduce intrapancreatic fat deposition (IPFD) in humans, synthesizing evidence from PubMed and Embase. The key finding was that lifestyle modification was associated with measurable reductions in IPFD compared with control conditions, supporting IPFD as a modifiable ectopic fat depot. Clinically, this strengthens the rationale for lifestyle-based metabolic interventions to potentially lower pancreatic disease risk linked to intrapancreatic fat.

Ahmad S, Sul HH, Danpanichkul P et al. · Current obesity reports · (2026) · View on PubMed ↗ · Free PDF ↗

Gut Metabolism Links Precision Nutrition, Exercise, and Healthspan in Drosophila melanogaster.

This Drosophila melanogaster study tested whether a multimodal precision nutrition and exercise regimen—chemically defined diet plus methionine restriction, taurine supplementation, and moderate exercise—extends healthspan and lifespan without functional trade-offs. The combination additively extended lifespan, preserved reproductive capacity, and improved locomotor function, and targeted metabolomics with stable isotope tracing indicated increased mitochondrial TCA cycle flux and improved gut redox homeostasis. Scientifically, it links gut metabolic remodeling to coordinated longevity and performance benefits, supporting metabolite-guided design of combined dietary and activity interventions.

Wei F, Liu S, Sun Y et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Durability and Safety of Imeglimin as an Add-On to DPP-4 Inhibitors in Japanese Type 2 Diabetes: The 104-Week FAMILIAR Trial.

This multicenter randomized placebo-controlled trial evaluated the long-term efficacy and safety of imeglimin as an add-on to DPP-4 inhibitors in Japanese adults with type 2 diabetes, including a focus on elderly patients, over 104 weeks (FAMILIAR trial). The primary endpoint was change in HbA1c from baseline to week 104, with meal tolerance tests and safety outcomes as secondary measures (full numerical findings truncated). Demonstrating durable glycemic control and acceptable safety for imeglimin plus DPP-4 inhibitors supports its use for long-term management in Japanese patients inadequately controlled on DPP-4 monotherapy.

Shimoda M, Osonoi T, Iwamoto M et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Peptide LKLKLL is a more effective component of Akkermansia muciniphila which regulate glucolipid metabolism through GLP-1/GIP dual modulation.

This preclinical study tested the hexapeptide LKLKLL derived from Akkermansia muciniphila for effects on glucolipid metabolism and incretin signaling in cell and mouse models. It found that LKLKLL improved metabolic outcomes in high-fat diet–induced obese and diabetic mice, including enhanced GLP-1 secretion and dual GLP-1/GIP modulation, alongside improved glucose tolerance and reduced body weight. These results position LKLKLL as a defined, translational alternative to live A. muciniphila for obesity/diabetes interventions targeting incretin pathways.

Li Y, Ye D, Fu C et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

Work-to-sleep ratio as a novel marker of NAFLD risk: evidence from U.S. and Korean national cohorts.

This cohort study assessed whether the work-to-sleep ratio (WSR)—a combined metric of occupational time relative to sleep recovery—predicts risk of NAFLD/MASLD using U.S. and Korean national cohorts. The key finding is that WSR functions as a novel behavioral marker associated with NAFLD risk beyond work hours or sleep duration alone. Clinically and public-health relevant, it suggests that balancing work demands with sleep recovery could be incorporated into risk stratification and prevention strategies for metabolic liver disease.

Zhong Y, Kou Y, Lu Z et al. · Nutrition & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Aging, Sleep & Frailty

Mechanism of actin thin filament pointed-end elongation by leiomodin.

This mechanistic study investigated how leiomodin (Lmod), particularly leiomodin-2 (Lmod2), promotes actin thin filament pointed-end elongation in striated muscle systems where actin exchange is normally biased to the pointed end. The key finding is that Lmod acts as an additional regulator of pointed-end actin filament growth, complementing known roles of nebulin (molecular ruler) and the pointed-end capping proteins tropomodulin (Tmod) and CapZ. This is significant for understanding how sarcomere actin length uniformity is maintained despite rapid turnover.

Brotzman SB, Palmer NJ, Boczkowska M et al. · Nature communications · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

Multidomain Lifestyle Intervention in Mild Cognitive Impairment: Subgroup Analysis of the SUPERBRAIN-MEET Randomized Trial.

This prespecified subgroup analysis of the 24-week SUPERBRAIN-MEET randomized controlled trial studied whether a multidomain lifestyle intervention (MLI) delivered via face-to-face sessions plus digital platforms improved cognition differently by sociodemographic factors, digital readiness, baseline cognitive status, and vascular risk in adults with mild cognitive impairment (MCI). The key finding was that the cognitive benefits of the MLI varied across these baseline subgroups, indicating differential responsiveness rather than uniform effects. These results support more tailored use of lifestyle-based dementia prevention strategies by identifying which MCI patients are most likely to benefit based on modifiable readiness and risk profiles.

Kim DA, Lee SM, Sun K et al. · Neurology · (2026) · View on PubMed ↗

Accelerated Epigenetic and Inflammatory Aging and Intrinsic Capacity.

This population-based cohort study examined cross-sectional and longitudinal associations between accelerated epigenetic and inflammatory aging and intrinsic capacity (IC), including domain-specific IC and sex differences, in older adults. The key finding was that accelerated epigenetic and inflammatory aging was associated with lower IC and predicted IC decline over time, with interactions between the two aging dimensions. These results advance preventive, function-oriented aging science by linking measurable molecular aging processes to real-world capacity loss.

Rouch L, De Souto Barreto P, Rolland Y et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Electroacupuncture Treatment on Sarcopenia in Patients Undergoing Maintenance Haemodialysis: An Effective Therapy.

This randomized controlled clinical study assessed whether electroacupuncture (EA) improves sarcopenia in patients undergoing maintenance haemodialysis (MHD). In 36 participants randomized to EA versus control, EA delivered 24 sessions over 8 weeks (30 minutes, three times per week) was evaluated for efficacy outcomes related to sarcopenia. If effective as reported, EA would represent a nonpharmacologic adjunct therapy for sarcopenia in the MHD population, potentially improving functional status and clinical management.

Chen R, Qian Q, Wang B et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Frailty mediates the association between sleep duration and physical, psychological, and cognitive multimorbidity in Chinese middle-aged and older adults.

This study used data from the China Health and Retirement Longitudinal Study (CHARLS) to test whether frailty mediates the association between sleep duration and physical, psychological, and cognitive multimorbidity (PPC-MM) in Chinese middle-aged and older adults. Using multivariate logistic regression and Cox proportional hazards models with restricted cubic spline (RCS) analysis, it found that sleep duration relates to PPC-MM risk and that frailty accounts for part of this relationship in both cross-sectional and longitudinal analyses. These findings highlight frailty as a potential intervention target linking sleep behaviors to multimorbidity risk in aging populations.

Ding H, Li L, Luo G et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmune/Inflammatory Disease Therapies & Guidelines

Genome-wide association analyses of borderline personality disorder identify 11 loci and highlight shared risk with mental and somatic disorders.

A genome-wide association study meta-analysis of borderline personality disorder (BPD) was conducted in European-ancestry participants (12,339 cases and 1,041,717 controls for discovery; 685 cases and 107,750 controls for replication). The study identified 11 independent risk loci and 9 risk genes, with SNP heritability of 17.3% and polygenic scores explaining 4.6% of BPD liability-scale variance. These findings improve genetic risk mapping for BPD and highlight shared susceptibility with both mental and somatic disorders, supporting cross-disorder biology.

Streit F, Awasthi S, Hall ASM et al. · Nature genetics · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Endothelial cell-intrinsic NOD2 signaling regulates the intestinal immune response through the generation of effector and memory T cells.

The authors investigated how endothelial cell-intrinsic NOD2 signaling regulates intestinal immunity by driving effector and memory T cell generation, focusing on the NOD2–muramyl dipeptide axis relevant to Crohn’s disease risk. They found that NOD2 engagement by muramyl dipeptide promotes T cell homing and differentiation programs that support intestinal immune responses and homeostasis. This provides a mechanistic explanation for how NOD2 variants can predispose to Crohn’s disease despite the immunostimulatory nature of its ligand.

Tsankov BK, Denney M, Ahn JSY et al. · Nature immunology · (2026) · View on PubMed ↗ · Free PDF ↗

The 2026 British Society for Rheumatology guideline for pain management in people with inflammatory arthritis.

The 2026 British Society for Rheumatology guideline was developed to address pain management in people with inflammatory arthritis (IA), drawing on evidence from electronic health record analyses, patient surveys, and trial evidence. It responds to observed overuse of long-term opioids and gabapentinoids despite limited trial efficacy and emphasizes underused non-pharmacological approaches with supportive evidence. This guideline provides an evidence-based, UK-specific framework to improve pain care and reduce reliance on ineffective long-term medications in IA.

Scott IC, Smith TM, Babatunde O et al. · Rheumatology (Oxford, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Caffeine and Cardiovascular Disease: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement reviewed evidence on caffeine intake and its associations with cardiovascular risk factors and cardiovascular disease across human observational studies and differing patterns of caffeine exposure. Overall findings suggest complex, heterogeneous effects with acute versus chronic differences and an inverse J-shaped relationship for naturally occurring caffeinated beverages in many studies. Clinically, the statement emphasizes that cardiovascular guidance should consider caffeine source, dose pattern, and individual susceptibility rather than assuming a uniform cardiovascular effect.

Marcus GM, Hu FB, van Dam RM et al. · Circulation · (2026) · View on PubMed ↗

Deucravacitinib in Active Psoriatic Arthritis: Efficacy and Safety up to 52 Weeks From the Randomized, Double-Blind, Phase 3 POETYK PsA-2 Trial.

The POETYK PsA-2 phase 3 randomized, double-blind trial evaluated deucravacitinib, an oral selective TYK2 inhibitor, in patients with active psoriatic arthritis (PsA) who were biologic-naïve or previously treated with tumor necrosis factor inhibitors. Over up to 52 weeks, patients were randomized to deucravacitinib 6 mg daily, placebo, or apremilast 30 mg twice daily (safety reference), with efficacy assessed using American College of Rheumatology response endpoints and safety tracked through week 52. If confirmed, these results would position deucravacitinib as a longer-term targeted oral option for PsA with a defined comparative safety/efficacy profile versus placebo and apremilast.

Mease PJ, Chandran V, Armstrong AW et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

Medical Students’ Attitudes, Perceptions, and Self-Reported Familiarity With Artificial Intelligence in Healthcare: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis synthesized studies reporting medical students’ attitudes, perceptions, and self-reported familiarity with artificial intelligence in healthcare. It highlighted that prior research used heterogeneous survey instruments and AI referents, and the authors emphasized construct harmonization, participant independence, heterogeneity, prediction intervals, risk of bias, and certainty of evidence. The findings are significant for designing AI literacy and curriculum interventions that match students’ measured baseline familiarity and attitudes across settings.

Zhang W, Han J, Han X et al. · JMIR medical education · (2026) · View on PubMed ↗ · Free PDF ↗

Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.

This systematic literature review examined reported associations between viral infections and antiviral vaccinations and the occurrence of autoimmune encephalitis (AIE), including anti-NMDAR and other AIE subtypes. The authors synthesized published case evidence to characterize which triggers are linked to specific AIE forms and how frequently they are reported across subtypes (full quantitative results are truncated). Clarifying infection/vaccine associations can inform risk assessment and mechanistic hypotheses about immunological triggers for AIE.

Bamberg S, Schulte-Frankenfeld PM, Kreye J · Brain, behavior, & immunity - health · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondria-targeted MXene-based nanozymes promote mitophagy and inhibit mtDNA-triggered cGAS/STING inflammation in osteoarthritis.

This preclinical study developed a mitochondria-targeted MXene-based nanozyme (MS@PMXene-TK with a mitochondria-targeting peptide MTP-131 and ROS-responsive thioketal PEG-TK shell) to treat osteoarthritis by promoting mitophagy and suppressing mtDNA-triggered cGAS/STING inflammation. The nanozyme platform was engineered to deliver a chondro-inductive peptide (SPPEPS) and to respond to ROS at the subcellular level, thereby enhancing mitophagy and inhibiting cGAS/STING-mediated inflammatory signaling (full efficacy data are truncated). This provides a mechanistically targeted nanotherapeutic strategy for OA that links mitochondrial quality control to innate immune pathway suppression.

Li T, Zheng A, Zhu C et al. · Bioactive materials · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting BLyS and APRIL with Telitacicept versus Conventional Immunotherapy in Generalized Myasthenia Gravis: A Comparative Study.

This retrospective real-world comparative study evaluated telitacicept versus conventional immunotherapy in patients with acetylcholine receptor antibody-positive generalized myasthenia gravis (AChR-Ab+ gMG), using 215 total patients (43 telitacicept, 172 conventional) and propensity score matching (1:1 to 35 per group). The study assessed treatment response based on changes in clinical outcome measures (details truncated in the abstract) and aimed to determine effectiveness and safety in a broader AChR-Ab+ population than prior trials. The findings are intended to validate telitacicept’s clinical utility and tolerability in routine practice for AChR-Ab+ gMG.

Yang Y, Kang N, Zhu Y et al. · ImmunoTargets and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluating the pharmacokinetics, efficacy and safety of low-dose cannabidiol.

This article reviewed pharmacokinetic (PK), pharmacodynamic (PD), and safety evidence for low-dose cannabidiol (CBD) at doses ≤2.5 mg/kg or ≤175 mg/day, including oral PK studies ≤150 mg. It found that low-dose CBD produces peak concentration (Cmax) and exposure (AUC) values 5- to 100-fold lower than those seen with a typical 20 mg/kg dose of Epidiolex, with PD studies showing little evidence of physical or neurological effects in healthy volunteers. The review is clinically significant because it contextualizes over-the-counter low-dose CBD recommendations and supports evidence-based expectations for exposure and effects at these lower doses.

Warren WG, Osborn M, Yates A et al. · British journal of clinical pharmacology · (2026) · View on PubMed ↗

Efficacy of magnesium-calcium ionic oral rinse for primary burning mouth syndrome: a randomized, double-blind, placebo-controlled trial.

This randomized, double-blind, placebo-controlled trial tested a magnesium–calcium ionic oral rinse for efficacy and safety in patients with primary burning mouth syndrome (BMS). The key finding was that the magnesium–calcium oral rinse improved symptoms compared with placebo while maintaining acceptable safety. This supports local modulation of the oral ionic microenvironment as a potential treatment approach for primary BMS with fewer systemic adverse effects.

Carrió N, Garawani BE, Alahmad A et al. · BMC oral health · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 26, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.