PubMed Trending Research Digest — June 07, 2026

Automated digest · 100 articles · 15 research areas · June 07, 2026

Overview

This week’s digest is dominated by mechanistic immunology and precision approaches—spanning cancer immune evasion, immune-cell state mapping, and targeted immunotherapies. Multiple studies highlight how tumors and immune systems interact through metabolism and microenvironmental constraints: e.g., HMGCS1-driven membrane repair shields tumors from cytotoxic lymphocytes, while fibroblast TXNDC5-mediated TGFβ signaling builds an immunosuppressive, PD-1–resistant barrier in colorectal cancer. On the therapeutic side, several CAR T advances (B7-H3 in cholangiocarcinoma, cathepsin-G–targeted AML CAR T, and antiviral TCR-primed CAR T strategies) aim to improve persistence and reduce antigen escape or off-target effects, while NKG2A blockade emerges as a rational strategy in defined tumor-associated NK cell subsets.

A second major thread connects neurobiology to systemic risk and inflammation. Work on microglia and astrocytes (CD31 in Alzheimer’s, Gal-3 in sepsis-associated encephalopathy, migrasome-enriched EVs after stroke, and astrocytic phenotypic switching in cancer pain) converges on glial control of synaptic function, network activity, and neuroinflammation as actionable targets. In parallel, several studies link endocrine/inflammatory biology and behavior to cardiometabolic and mental health outcomes—ranging from time-use and chronotype pathways linking depression to CVD, to inflammation–hormone/vitamin D associations, and to ferroptosis-related immune-cell genetics for depression risk.

Finally, the week includes translational and clinical-implementation momentum: kidney disease trials and pooled analyses extend finerenone benefits beyond diabetes, while multiple consensus guidelines (CLL/SLL, RA-ILD, perioperative ERAS, and invasive CSCC) aim to standardize care. Across domains, improved biomarkers and risk prediction—using proteomics, imaging, routine blood indices, and machine learning—signal a broader shift toward scalable, mechanism-informed stratification to guide therapy and monitoring.

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Cancer immunotherapy (CAR T, bispecifics, immune checkpoint)

Engagement of the TCR against an oncolytic virus generates a population of effector CAR T cells with potent antitumor activity.

This study examined how engaging the endogenous T cell receptor (TCR) against an oncolytic virus shapes CAR T cell populations and function, using CAR T cells combined with vesicular stomatitis virus (VSV) in solid tumor models. The combination generated a subpopulation of antiviral, TCR-primed effector CAR T cells with enhanced effector functions, durability, and distinct gene/protein expression compared with non-TCR-primed CAR T cells, supported by single-cell RNA sequencing showing clonal expansion of anti-VSV CAR T cells. The findings are significant for improving CAR T cell performance against solid tumors by leveraging oncolytic-virus-driven TCR engagement to reduce exhaustion and enhance persistence.

Liseth O, Appleton E, Kendall B et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Cytotoxic CD39+ tumor-associated NK cells respond to NKG2A blockade in lung cancer.

This study characterized tumor-infiltrating natural killer (NK) cell states in non-small cell lung cancer (NSCLC) and tested responsiveness to NKG2A blockade, using matched single-nucleus RNA and ATAC sequencing from patient samples. It identified two tumor-associated NK (taNK) subsets marked by ITGAE (CD103) and ITGA1 (CD49a) that show tissue-residency and dysfunction features while retaining cytotoxic function, and it reported that cytotoxic CD39+ taNK cells respond to NKG2A blockade. Clinically, these data support NKG2A-targeted immunotherapy and suggest CD39+ cytotoxic taNK cells as a functional biomarker for response in lung cancer.

Serger C, Rebuffet L, Sandholzer MT et al. · Science immunology · (2026) · View on PubMed ↗ · Free PDF ↗

High-avidity cathepsin-G-specific CAR-T cells for the treatment of acute myeloid leukemia.

The study developed and tested high-avidity cathepsin-G–specific CAR T cells (CG1.CAR-T) for acute myeloid leukemia (AML) targeting an HLA-A*02:01–restricted cathepsin-G peptide. CG1.CAR-T cells were engineered to co-express LCK and duplicate CD3ζ, enabling functional recognition of the CG1 peptide at low concentrations (as low as 0.025 mM). This work supports a strategy to improve AML CAR T potency while potentially reducing off-target depletion of normal myeloid progenitors by using a myeloid-restricted antigen and enhanced signaling avidity.

Dotti G, Walhart T, Biondi M et al. · Blood · (2026) · View on PubMed ↗

Sustained moderate to high triglyceride-glucose index level is associated with a lower risk of sarcopenia in middle-aged and elderly adults: a nationally representative cohort study.

In two CHARLS subcohorts totaling 6,033 Chinese adults aged ≥45, the study examined associations between baseline TyG index, cumulative TyG index, and TyG index subgroup patterns (two time-point measurements) and incident sarcopenia. Sustained moderate-to-high TyG index levels were associated with a lower risk of developing sarcopenia. This suggests that longitudinal insulin-resistance surrogates based on TyG may help identify sarcopenia risk trajectories in middle-aged and elderly populations.

Li Z, Zhu Z, Chen L et al. · Lipids in health and disease · (2026) · View on PubMed ↗ · Free PDF ↗

B7-H3 CAR T cells eradicate intrahepatic cholangiocarcinoma and induce durable response.

This preclinical study evaluated B7-H3–targeted CAR T cells generated from peripheral blood mononuclear cells of normal donors and transduced with a retroviral vector encoding a second-generation CAR, testing efficacy against intrahepatic cholangiocarcinoma (ICC) in vitro and in vivo. B7-H3 CAR T cells eradicated intrahepatic cholangiocarcinoma and produced durable responses in the experimental models. The work supports B7-H3 as a viable target and provides rationale for CAR T development in advanced ICC.

Arya S, Ventin M, Cattaneo G et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer biology & tumor microenvironment (metabolism, fibrosis, immune evasion)

HMGCS1 drives cholesterol-dependent membrane repair and shields tumor cells from lymphocyte attack.

This study identified how tumor metabolism enables resistance to cytotoxic lymphocytes by focusing on hydroxymethylglutaryl-CoA synthase 1 (HMGCS1) in cancer cells. Through a functional screen of 111 metabolic enzymes, HMGCS1 was found to drive cholesterol-dependent plasma membrane repair after perforin-induced damage, shielding tumors from NK cells, CAR-T cells, and anti-PD-1 therapy. These results position HMGCS1/cholesterol synthesis as a potential metabolic vulnerability to enhance immunotherapy efficacy.

Zhang Y, Wang S, Luo T et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Glycobiology-driven therapeutic targeting of glycan-binding proteins: mechanisms, diseases, and clinical translation.

This review studied how galectin glycan-binding proteins can be therapeutically targeted across diseases such as cancer, cardiovascular disorders, neurodegeneration, metabolic disorders, and autoimmune conditions. It reports that despite conserved carbohydrate recognition domains, individual galectins show context-dependent functions that can be exploited for clinical translation using glycobiology-driven targeting strategies. The work is significant because it provides a mechanistic framework for developing next-generation galectin-targeted therapies aimed at immune evasion, fibrosis, metastasis, and cell-fate control.

Popatia AM, Sharanek A, Jahani-Asl A · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting fibroblast TXNDC5 resolves tumor desmoplasia and PD-1 resistance in colorectal cancer with mesenchymal traits.

This study investigated the role of the fibroblast protein TXNDC5 (a protein disulfide isomerase) in colorectal cancer, including colorectal cancer-associated fibroblasts in human and mouse models, and its impact on immunotherapy response. It found that TXNDC5 enhances TGFβ signaling by stabilizing the TGFβ receptor TGFBR1, driving fibroblast activation, tumor desmoplasia, and resistance to PD-1 blockade, while fibroblast-specific Txndc5 deletion reduced tumor stiffness, improved vessel function, decreased hypoxia, and inhibited immunosuppressive barrier formation. The results are significant because they identify TXNDC5 as a targetable regulator of the fibrotic immune-exclusion niche that can potentially restore PD-1 immunotherapy efficacy in mesenchymal-type colorectal cancer.

Cheng KL, Chen CI, Yu SH et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

TSC22D4 drives clear cell renal cell carcinoma progression and therapy resistance by stabilizing NRF2 through KEAP1 disruption.

This study examined how TSC22D4 contributes to clear cell renal cell carcinoma (ccRCC) progression and therapy resistance by regulating NRF2 stability through disruption of KEAP1. It identified TSC22D4 as a KEAP1-interacting protein that stabilizes NRF2, thereby promoting oxidative-stress response programs including proliferation and metabolic reprogramming while supporting ferroptosis resistance. The findings are significant because they nominate the TSC22D4–KEAP1–NRF2 axis as a potential therapeutic vulnerability in ccRCC.

Zeng B, Wang S, Zhang X et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

The Gdf15-xenobiotic receptor axis shapes NK cell maladaptation predicting cold tumors under environmental stress.

This study investigated the Gdf15–xenobiotic receptor (AhR) axis in epithelial ovarian cancer (EOC) and how it shapes NK cell maladaptation under environmental stress, using clinical and cellular analyses. It found that EOC cell-derived Gdf15 facilitates AhR signaling in the tumor immune niche and that AhR signaling becomes enriched in NK cells following chemotherapy, contributing to NK maladaptation in cold tumors. The work is significant because it links a tumor-secreted factor (Gdf15) to xenobiotic receptor signaling (AhR) as a mechanism predicting immune failure in harsh, low-infiltration tumor environments.

Kim J, Kim KH, Du Z et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting the METTL1/m⁷G axis as a therapeutic strategy in myeloid leukemia.

This study investigated the therapeutic potential of targeting the METTL1/m⁷G (N7-methylguanosine) axis in myeloid leukemia, focusing on leukemia stem cell (LSC) self-renewal and homing in the bone marrow microenvironment. METTL1 was identified as a key regulator of LSC maintenance by catalyzing m7G formation on the specific tRNA tRNAPheGAA, and METTL1 loss reduced m7G abundance, suppressed translation, and promoted degradation of transcripts enriched with tRNA-dependent features. The findings are significant because they nominate METTL1-mediated m7G/tRNAPheGAA as a druggable vulnerability for disrupting LSC-driven leukemogenesis.

Ren L, Zhang H, Bobileva O et al. · Blood · (2026) · View on PubMed ↗

Immunotherapy rechallenge in gastric cancer: resistance mechanisms, molecular stratification, and precision decision-making.

This narrative review studies immune checkpoint inhibitor (ICI) resistance mechanisms and the rationale for immunotherapy rechallenge in advanced gastric cancer (GC) patients who initially respond and then progress. It summarizes resistance pathways including tumor-intrinsic plasticity, hypoxia/metabolism-driven tumor remodeling, impaired antigen presentation, an immunosuppressive tumor microenvironment, T-cell exhaustion, and compensatory checkpoint signaling (e.g., Lymphocyte-activation gene 3 and related axes). The review supports molecular stratification and precision decision-making to identify which GC patients may benefit from ICI rechallenge after acquired resistance.

Jiang YC, Zheng LL, Fu MG et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Reversing Bladder Cancer Chemo-resistance through Blocking Cell Senescence by a Combination Therapy.

This Theranostics study investigates reversing bladder cancer chemo-resistance by blocking cell senescence using combination therapy in drug-refractory bladder cancer models. It analyzes HDAC1–3 expression in tumor tissues to relate epigenetic drivers to chemoresistance programs, then tests a co-delivery strategy combining the pan-HDAC inhibitor belinostat (PXD101) with paclitaxel (PTX) in patient-derived cancer models. The results support senescence-targeting epigenetic therapy as a strategy to restore chemotherapy sensitivity in advanced bladder cancer.

He Y, Fang Z, Zhang J et al. · Theranostics · (2026) · View on PubMed ↗ · Free PDF ↗

Primary Cilium Forces Neuroendocrine Shift in Prostate Cancer through YAP1 Repression and Reduced Mitochondrial Activity.

The study examined how primary cilia regulate neuroendocrine (NE) plasticity in prostate cancer, analyzing cilia distribution in vitro and in castration-resistant prostate cancer (CRPC) patient tumor samples and mouse models. Primary cilia were detected in NE-like cells (absent in localized hormone-sensitive tumor cells) and were associated with FDG-PET positivity, NE features, YAP1 repression, and reduced mitochondrial activity/metabolic reprogramming. These findings suggest ciliogenesis as a mechanistic driver of CRPC metabolic and transcriptional shifts and a potential therapeutic vulnerability in NE prostate cancer.

Guo Y, Peng S, Jamet T et al. · Theranostics · (2026) · View on PubMed ↗ · Free PDF ↗

The molecular architecture of tunneling nanotubes.

This preprint studied tunneling nanotubes (TNTs) and aimed to define their morphology and function using experimental systems that overcome light-microscopy limitations. The authors established two complementary approaches to stimulate TNT formation and to quantify TNT-mediated transfer, including a viral-kinase–based induction using the pseudorabies virus US3. By providing clearer criteria and functional assays for TNTs, the work supports mechanistic studies of TNT roles in tumor biology, chemotherapy resistance, and virus-enhanced intercellular spread.

Karasmanis EP, Chen S, Shaikh F et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer genomics & precision oncology (CRISPR, molecular classification, biomarkers)

Multiplexed, precise genome engineering in monocots with twin prime editing systems.

This study developed a twin prime editing-based knockout (TKO) system to enable multiplexed, precise genome engineering in monocots (rice, maize, and hexaploid wheat). The TKO approach installs stop codon clusters for translational termination with reduced in-frame mutations, achieving high knockout efficiencies (up to ~70.5% in rice protoplasts) and heritable knockouts in regenerated rice, while outperforming Cas9 for certain triple-homolog knockouts in wheat. The ability to use orthogonal TKO editors to simultaneously knock out up to ten genes provides a powerful platform for rapid functional genomics and crop trait engineering.

Li H, Chai Z, Shi X et al. · Nature biotechnology · (2026) · View on PubMed ↗

Artificial intelligence for the prediction of prognosis in colorectal cancer patients using routine blood indices.

This multicenter study used explainable machine learning to predict overall survival in colorectal cancer (CRC) patients using routine blood indices, training on 850 patients and validating on 403 and 217 patients from independent cohorts. Random survival forest (RSF) models performed best among evaluated time-to-event approaches, with SHAP used for interpretability. The results suggest that routinely collected blood tests can support clinically actionable, explainable prognostic risk stratification in CRC without requiring specialized assays.

Tian S, Li J, Liu Q et al. · NPJ digital medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Clinical relevance of CA125 in low-grade serous ovarian cancer: a retrospective multi-center JAGO/NOGGO study.

This retrospective multi-center JAGO/NOGGO study evaluated the clinical relevance of CA125 measured at predefined time points for survival and recurrence detection in low-grade serous ovarian cancer. It analyzed serial CA125 levels from diagnosis through post-debulking, adjuvant therapy, follow-up, and recurrence in patients treated between 2007 and 2023 across 9 tertiary centers in Germany and Austria. The significance is that it clarifies whether CA125 can serve as a prognostic biomarker and guide recurrence monitoring in this specific ovarian cancer subtype.

Flethe C, Netkova-Heintzen M, Postl M et al. · International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · (2026) · View on PubMed ↗ · Free PDF ↗

Deep learning for H&E-based meningioma molecular classification and outcome prediction: a retrospective cohort study.

This retrospective multicentre study evaluated whether deep learning applied to haematoxylin and eosin (H&E)–stained meningioma tissue can perform molecular classification and predict clinical outcomes. It aimed to robustly identify meningioma molecular subtypes, predict recurrence risk, and detect salient chromosome copy number alterations from routine pathology images. The significance is that it could enable genome-informed risk stratification without requiring separate genomic profiling, improving scalability of precision oncology for meningioma patients.

Landry AP, Nassiri F, Yefet LS et al. · The Lancet. Digital health · (2026) · View on PubMed ↗ · Free PDF ↗

Long-Term Outcomes of Plastic Versus Metal Stents for Preoperative Biliary Drainage in Pancreatic Cancer: A Nationwide Propensity Score-Matched Analysis.

In a nationwide propensity score-matched analysis of patients with pancreatic ductal adenocarcinoma undergoing curative-intent surgery, this study compared long-term outcomes after preoperative biliary drainage using plastic stents versus metal stents (via ERCP) before pancreaticoduodenectomy. Metal stents and plastic stents differed in overall survival and recurrence-free survival over long-term follow-up, informing which stent type may be preferable in the neoadjuvant-therapy era. These data help refine endoscopic management decisions for obstructive jaundice in PDAC patients prior to surgery.

Nagai K, Hirakawa S, Mizuma M et al. · Gastrointestinal endoscopy · (2026) · View on PubMed ↗

Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.

This preclinical study identified covalent inhibitors that irreversibly inactivate the human papillomavirus type 16 (HPV-16) E6 oncoprotein by targeting a cysteine near the E6AP-binding interface, and tested their effects in HPV-driven tumors in vivo. Covalent E6 inhibition restored p53 stability and transcriptional activity, induced apoptosis and senescence in HPV-16-positive cancer cells, and spared HPV-negative epithelial cells, with CRISPR-engineered E6 cysteine-to-serine knock-in abolishing the effect. The work is significant as a genotype-defined therapeutic strategy that directly targets HPV-16 E6 to reverse the p53 degradation dependency in HPV-associated cancers.

Rietz A, Kumari L, Koirala A et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

IRF2 is an Essential Transcription Factor with Pathogenic and Prognostic Impact in Multiple Myeloma.

The study used a CRISPR-Cas9 library screen in multiple myeloma (MM) cells to identify essential transcription factors and then mapped IRF2 chromatin binding using Cut&Run. IRF2 emerged as a critical MM driver alongside IRF family members, with extensive IRF2 binding to chromatin occurring both independently and cooperatively with IRF1 and IRF4. These findings position IRF2 as a pathogenic and prognostic regulator and suggest it as a potential therapeutic target in MM transcriptional programs.

Gómez-Echarte N, Carrasco-Leon A, Maiques-Diaz A et al. · Blood · (2026) · View on PubMed ↗

CRISPR activation of endogenous PKD1 increases polycystin-1 levels and suppresses cellular features of ADPKD.

This preprint studied CRISPR activation (CRISPRa) of the endogenous PKD1 gene to increase polycystin-1 (PC1) levels and suppress cellular phenotypes relevant to autosomal dominant polycystic kidney disease (ADPKD). Using an EGFP-reporter–guided sgRNA screen, the authors identified proximal PKD1 promoter–targeting single guides that increased endogenous Pkd1 mRNA in mouse collecting duct-derived Pkd1 RC/- cells and in human cell models. The work supports transcriptional upregulation of PKD1 as a gene-dosage–restoring strategy for ADPKD.

Chakraborty A, Varghese MM, Wallace DP et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

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Virology & antiviral mechanisms (including vaccine/structural virology)

Early immune events during SARS-CoV-2 infection impact memory T and B cell responses.

This longitudinal cohort study investigated early immune events during SARS-CoV-2 infection that shape later memory T and B cell responses in 46 hospitalized COVID-19 patients. Using RNA-seq, targeted proteomics, and flow cytometry, the authors linked early immune signatures to variability in the magnitude and quality of post-infection memory immunity up to one year. The findings improve mechanistic understanding of why patients develop different durable immune responses and could inform biomarkers or interventions to optimize long-term protection.

Woloszczuk K, Joyner D, Connors J et al. · Communications biology · (2026) · View on PubMed ↗ · Free PDF ↗

Cryo-EM structures of Měnglà virus GP reveal combined Ebola- and Marburg-like epitope masking strategies for antibody evasion.

This structural virology study used cryo-electron microscopy (cryo-EM) to determine how the Měnglà virus (MLAV) glycoprotein (GP) evades antibodies, including in complex with the MARV-neutralizing antibody MR191. The MLAV GP structures revealed combined Ebola- and Marburg-like epitope masking strategies, including distinctive Wing and heptad repeat 1D (HR1D) features, retention of a visible Cap structure after protease treatment, and a MARV GP-like α2 helix. These results are significant for understanding cross-filovirus immune evasion and for guiding design of broadly neutralizing antibodies or vaccines targeting MLAV.

Wang L, Zou B, Liu B et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

TurboID-Based Proximity Labeling Map Reveals the Protein Interaction Network and Anti-Viral Mechanism Against Influenza A H1N1.

The study used TurboID-based proximity labeling to map protein interaction networks of 10 influenza A H1N1 viral proteins in human alveolar epithelial A549 cells. Hemagglutinin (HA) and polymerase acidic (PA) were found to directly bind MAVS and suppress IFN-β promoter activation, with interaction validation using co-immunoprecipitation, confocal microscopy, and dual-luciferase reporter assays plus functional tests. This delineates a specific viral-host anti-viral mechanism targeting MAVS–IFN signaling and identifies interaction nodes that could be exploited for antiviral therapy.

Wang M, Wang Z, Liu C et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Why Andes hantavirus is not the next SARS-CoV-2: contrasting viral shedding, transmissibility and genomic patterns.

This article analyzed why Andes hantavirus is unlikely to become the next SARS-CoV-2 by contrasting viral shedding, transmissibility, and genomic patterns in the context of a cruise ship-associated outbreak. It concludes that Andes virus differs fundamentally from SARS-CoV-2 because it is rodent-borne with vascular pathogenesis, diagnosis relies on blood PCR and serology, and genomic diversity is driven more by reservoir ecology and geography than sustained human-to-human transmission. The comparison is significant for public health risk assessment by clarifying which viral features drive pandemic potential.

Bal A, Sauvage V, Bouscambert-Duchamp M et al. · Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · (2026) · View on PubMed ↗ · Free PDF ↗

Cross-reactive Bundibugyo antibody responses after licensed Ebola vaccines.

This preprint investigates whether licensed Ebola vaccines induce cross-reactive antibody responses against Bundibugyo virus (BDBV) in participants from the PREVAC randomized clinical trial. Using a multiplex Luminex assay on serum collected at day 28 (D28) and month 3 (M3) after vaccination with rVSVΔG-ZEBOV-GP or Ad26.ZEBOV/MVA-BN-Filo, it assesses cross-reactivity to filovirus glycoproteins including BDBV. Demonstrating cross-reactive immunity would inform vaccine strategy for outbreaks where no BDBV-specific licensed vaccine is available.

Lhomme E, Wiedemann A, Ayouba A et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Phage RyR-domain proteins degrade ADPR-based immune signals and fuel NAD + synthesis.

This study investigated how bacteriophage proteins terminate NAD+-based immune signaling by degrading cyclic ADP-ribose molecules in the Thoeris anti-phage defense system. Through a forward biochemical screen, the authors identified the mycobacteriophage RyDEP as an enzyme that cleaves 2’cADPR and 3’cADPR, thereby shutting down immune activation. These findings reveal a specific viral countermeasure to nucleotide immune signals and clarify a mechanism that could inform anti-phage and host-defense biology.

López Rivera M, Chang RB, Lewis CM et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroscience & neurodegeneration (Alzheimer’s/ALS/PD, synapses, glia, neuroinflammation)

Microglial galectin-3 disrupts parvalbumin interneurons and hippocampal synchrony, driving cognitive deficits.

Using a lipopolysaccharide (LPS)-induced mouse model of sepsis-associated encephalopathy, this study examined how microglial galectin-3 (Gal-3) affects parvalbumin interneurons and hippocampal synchrony to drive cognitive deficits. Systemic LPS upregulated microglial Gal-3, which activated Toll-like receptor 2 (TLR2) signaling and promoted NLRP3/AIM2 inflammasome-related pathways, disrupting parvalbumin interneuron function and network synchrony. These results position microglial Gal-3 as a mechanistic driver and potential therapeutic target for preventing cognitive impairment after sepsis.

Jia M, Shao H, Ma SQ et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Quantitative tandem mass tag-based serum proteomics for longitudinal biomarker monitoring in Duchenne muscular dystrophy.

This study used tandem mass tag (TMT)-based serum proteomics to quantify longitudinal protein changes in patients with Duchenne muscular dystrophy (DMD) and relate them to motor function performance. The authors identified serum proteins associated with motor function trajectories, enabling blood-based monitoring that could detect disease-related changes beyond conventional motor tests. These findings support TMT serum proteomics as a scalable biomarker strategy for improving sensitivity in DMD clinical trials and longitudinal disease management.

Naveed A, Recinos E, Chow D et al. · Clinical proteomics · (2026) · View on PubMed ↗ · Free PDF ↗

Cryo-EM structures of heteromeric Kir4.1/5.1 channel suggest mechanisms of inward rectification and channel blockage.

This structural biology study used cryo-electron microscopy to determine conformations of the heteromeric Kir4.1/Kir5.1 inwardly rectifying potassium channel in apo form and in complex with spermine and inhibitors including VU0134992 and EHop-016. The reported structures clarify mechanisms of inward rectification and how polyamines block the channel, including insights relevant to EAST/SeSAME syndrome caused by Kir4.1/5.1 dysfunction. The work provides a mechanistic framework for rational design of modulators targeting Kir4.1/5.1 in neurological and renal disorders.

Ning Y, Zhou X, Zhang Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in 5×FAD mice.

This study examined the role of microglial CD31 in Alzheimer’s disease using human data and 5×FAD mice. Microglia-specific CD31 knockdown reduced dysregulated transcriptional programs, suppressed microglial hyperactivation and disease-associated microglia (DAM), decreased amyloid-β deposition and inflammation, and improved cognition. Mechanistically, the authors implicate altered recruitment/signaling involving Src homology phosphatase 2 (SHP2), suggesting CD31 as a therapeutic target to mitigate AD pathology.

Zhou Q, Sun F, Zhang Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

TDP-43 oxidation and PP1 crosstalk at RNA granule-mitochondria contact sites.

This study examined how mitochondrial oxidative phosphorylation (OXPHOS) regulates RNA granule–mitochondria contact formation and the behavior of the RNA-binding protein TDP-43 in cells, using super-resolution live microscopy. It found that ROS generated by mitochondrial OXPHOS promote TDP-43 localization to cytoplasmic RNA granules via cysteine oxidation at Cys173/Cys175, with tethering mediated by TDP-43 binding to GADD34 on mitochondria. The findings are clinically and scientifically important because they link mitochondrial redox state to TDP-43 mislocalization mechanisms relevant to neurodegenerative disease pathology.

Ball HE, Woods AC, Wong YC · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

HM568 Enhances NAD+ Biosynthesis to Ameliorate Mitochondrial Dysfunction and Neurotoxicity in Parkinson’s Disease Models: A Putative Link to PARP1 Modulation.

The study tested the compound HM568 in Parkinson’s disease (PD) models induced by MPTP/MPP+ to determine whether it improves mitochondrial dysfunction and neurotoxicity and to explore a link to PARP1 modulation. HM568 improved behavioral deficits, preserved dopaminergic neurons, restored blood-brain barrier integrity, and normalized mitochondrial morphology, while proteomics implicated mitochondrial respiratory chain complexes and cellular assays showed HM568 counteracted MPP+-induced inhibition of complexes I, III, and IV. This supports HM568 as a mitochondria-targeting candidate that may mitigate PD pathology through pathways related to PARP1 overactivation.

Li M, Li W, Liu Y et al. · Molecular neurobiology · (2026) · View on PubMed ↗

The microbiota-tryptophan-brain axis in neurodegenerative diseases: pathogenic mechanisms, disease-specific roles, and translational therapeutics.

This review studies the microbiota–tryptophan–brain axis in neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), focusing on disease-specific roles and translational therapeutics. It links gut microbial metabolism of tryptophan through indole, kynurenine (KYN), and serotonin pathways to CNS effects via the microbiota–gut–brain axis, including immune and neurobiological mechanisms. The article highlights tryptophan-metabolite pathways as potential biomarkers and therapeutic targets for neurodegenerative disease modulation.

Wang Z, Li L, Dong Y et al. · Frontiers in microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Hyperoside protects against poly-GR-mediated neurodegeneration via regulation of mitochondrial fission and oxidative stress in C9orf72-associated ALS.

This study tested whether hyperoside, a flavonoid, mitigates poly-GR–mediated mitochondrial dysfunction and oxidative stress in C9orf72-associated ALS using motor neuron-like cells and an AAV-m in vivo model. Hyperoside attenuated poly-GR–driven mitochondrial injury and oxidative stress and improved neuronal survival in both experimental systems. The results support hyperoside as a potential therapeutic candidate targeting C9orf72 poly-dipeptide–induced neurodegeneration mechanisms.

Hsieh WC, Lin CY, Wu HC et al. · Chinese medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Tau extent outperforms tau load as a predictor of neurodegeneration in Alzheimer’s disease.

In 367 participants spanning healthy aging to Alzheimer’s disease in the TRIAD cohort, the study compared how tau-PET spatial extent of tauopathy (SEOT) versus tau load predicts neurodegeneration cross-sectionally and longitudinally, using [18F]MK-6240 tau-PET. Tau extent (SEOT) outperformed tau load as a predictor of neurodegeneration. This improves biomarker selection for staging and prognosis in Alzheimer’s disease by emphasizing spatial spread of tau pathology over regional burden.

Macedo AC, Trudel L, Hosseini SA et al. · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

MOTS-c: How a secreted mitochondrial microprotein may become a potential treatment for inflammatory lung diseases.

This review article synthesized experimental and clinical evidence on MOTS-c, a mitochondrial-derived secreted microprotein (mitokine) encoded within the 12S rRNA gene, and its potential therapeutic relevance to inflammatory lung diseases. The authors conclude that MOTS-c modulates oxidative/toxic stress, mitochondrial dysfunction, inflammation, and multiple cell-death pathways that are central to acute and chronic respiratory disorders, with evidence that circulating MOTS-c levels are reduced in acute respiratory distress. The review highlights MOTS-c as a mechanistically grounded candidate for future translational interventions in inflammatory lung disease.

Amado CA, Agüero J, García-Unzueta M et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

M2 microglia-derived migrasome-enriched extracellular vesicles restore mitochondrial homeostasis to orchestrate neurovascular unit recovery after ischemic stroke.

The study tested whether migrasome-enriched extracellular vesicles (EVs) derived from M2 microglia restore mitochondrial homeostasis and promote neurovascular unit recovery after ischemic stroke using OGD/R cell models and MCAO mice. M2 microglia-derived migrasome-enriched EVs were internalized by microglia, astrocytes, neurons, and microvascular endothelial cells and improved mitochondrial homeostasis, supporting neurovascular recovery. These results position migrasome-enriched EVs as a promising EV-based strategy to counter neuroinflammation-driven damage after ischemic stroke.

Zhang Y, Wu J, Liu L et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

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Pain & neuropsychiatric comorbidity (cancer pain, depression, suicidality, autism-like behavior)

Dissecting Immune Cell Ferroptosis via Single-Cell Multi-Omics Identifies RPL8 as a Potential Therapeutic Target for Depression.

This study used two-sample Mendelian randomization (MR) with blood cis-eQTLs (eQTLGen/GTEx) and depression GWAS (FinnGen), single-cell eQTL mapping in peripheral immune cells (OneK1K), and in silico docking to identify immune-cell ferroptosis genes relevant to depression. MR implicated 42 ferroptosis genes, and replication across cohorts highlighted ribosomal protein RPL8 as a protective factor against depression. Identifying RPL8 as a potential therapeutic target provides a gene-level, immune-cell-specific route for developing ferroptosis-modulating interventions for depression.

Zhang G, He R, Du B et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Neural SMG7 deficiency induces autism-like behaviours via PKD1 upregulation.

This study investigated whether neural Suppressor with morphogenetic effect on genitalia 7 (Smg7) deficiency causes autism-like behaviors by using an Emx1-Cre-mediated conditional Smg7 knockout mouse model (Smg7cko) in both male and female mice. The work reports that Smg7 loss induces autism-like phenotypes associated with increased PKD1 expression (PKD1 upregulation). Linking NMD-factor Smg7 to PKD1-driven neurobehavioral changes supports a mechanistic autism susceptibility pathway involving impaired RNA surveillance.

Pang Y, Hao A, Han H et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗

Astrocyte-specific NRCAM deficiency promotes GABAergic synapse pruning to drive central sensitization in bone cancer pain.

In a mouse model of bone cancer pain created by intrafemoral inoculation of fibrosarcoma cells, this study tested whether astrocyte-specific deficiency of neuronal cell adhesion molecule NRCAM promotes GABAergic synapse pruning and central sensitization. The authors focused on astrocyte-mediated synaptic phagocytosis, proposing that loss of astrocytic NRCAM removes an anti-phagocytic constraint on perisynaptic astrocytic processes. If confirmed, targeting astrocytic NRCAM-dependent synaptic pruning could offer a strategy to reduce central sensitization in bone cancer pain.

Zhang Z, Hou Y, Mao Y et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Associations between retinal morphological features and risk of depression and anxiety disorders.

This UK Biobank cohort study assessed whether optical coherence tomography (OCT) retinal morphological features are associated with incident depression and anxiety disorders in participants aged 40–70 years who underwent retinal OCT at recruitment. Baseline retinal layer measurements (e.g., RNFL, GCIPL, INL, and photoreceptor-related metrics) were used to model risk of developing depression and anxiety. If retinal morphology predicts psychiatric outcomes, OCT-based screening could enable earlier identification of individuals at elevated risk for depression and anxiety.

Li Y, Zhang Y, Yim C et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Suicidal ideation in patients with skin conditions: A multicentre European study.

This multicentre European cross-sectional study assessed suicidal ideation among dermatology outpatients across multiple skin conditions and analyzed sociodemographic, clinical, and psychological correlates. It found that suicidal ideation prevalence varies by dermatologic condition and is associated with factors such as psychological distress (e.g., depression/anxiety) and skin-related burdens. The findings are significant because they quantify suicidality risk in routine dermatology care and identify targets for screening and intervention.

Sampogna F, Abeni D, Schut C et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗

Neuroinflammatory mechanisms and pharmacological advances in autism spectrum disorder: from inflammatory pathways to targeted interventions.

This review synthesizes evidence on neuroinflammatory mechanisms in autism spectrum disorder (ASD) and discusses pharmacological advances targeting inflammatory pathways across clinical immune/CNS studies, cerebrospinal fluid findings, neuroimaging, animal models, and multi-omics. It emphasizes body-to-brain signaling from maternal immune activation (MIA) during pregnancy to postnatal immune imbalance and subsequent amplification of inflammatory signals in the brain. Mechanism-organized intervention points are proposed to help develop more targeted, potentially biomarker-guided therapies for ASD.

Zhang X, Xue H, Zhu C et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and safety of BCMA- or GPRC5D-directed CD3 bispecific antibodies in relapsed/refractory multiple myeloma: a systematic review and meta-analysis of prospective clinical trials and real-world studies.

This systematic review and meta-analysis evaluates BCMA×CD3 and GPRC5D×CD3 bispecific antibodies in relapsed/refractory multiple myeloma (RRMM) using data from prospective clinical trials and real-world studies. It finds and synthesizes efficacy outcomes such as progression-free survival (PFS) and response rates (e.g., stringent complete response, complete response, and ≥VG), alongside safety results, to estimate overall benefit and certainty of evidence. The results support evidence-based selection of BCMA- or GPRC5D-directed T-cell-redirecting therapies for RRMM patients.

Li J, Abulaiti A, Li D et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Astrocytic Phenotypic Switching in Posterior Piriform Cortex Orchestrates Bone Cancer Pain-Depression Comorbidity via Purinergic-Noradrenergic Signaling.

This study examined astrocytic phenotypic switching in the posterior piriform cortex in a mouse model of Lewis lung carcinoma to explain bone cancer pain with comorbid depression. Using metabolomics, proteomics, and fiber photometry, the authors reported that astrocytes transition from an A2 neuroprotective state to an A1 neurotoxic state and that this switch drives pain-depression comorbidity via purinergic–noradrenergic signaling. The findings identify a specific astrocyte-neuron signaling axis as a potential target for treating both affective and nociceptive components of cancer pain.

Liu JP, Zhang JH, Tan ZX et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Diagnostic tests and headache misdiagnoses in individuals with resistant and refractory migraine - data from the REFINE study.

The REFINE study analyzed baseline cross-sectional data from adults with episodic or chronic migraine in 15 European tertiary headache centers to compare resistant migraine (ResM) and refractory migraine (RefM) versus non-resistant/non-refractory migraine (NRNRM) regarding diagnostic testing history and misdiagnoses. Individuals with ResM/RefM reported more diagnostic tests and more headache misdiagnoses than those with NRNRM. These findings suggest that diagnostic pathways and diagnostic accuracy are major modifiable contributors to treatment delays and potentially worse outcomes in difficult-to-treat migraine.

De Santis F, Rosignoli C, Onofri A et al. · Cephalalgia : an international journal of headache · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiometabolic disease & lifestyle risk (obesity, diabetes, inflammation, time-use, chronotype, TyG)

A body roundness index (BRI)-based predictive model for metabolic syndrome in perimenopausal and postmenopausal women-from a cross-sectional machine learning study to a longitudinal dynamic assessment.

This study developed a Body Roundness Index (BRI)-based machine-learning prediction model for metabolic syndrome in perimenopausal and postmenopausal women using NHANES 2007–2020 for training and an external validation cohort from the Affiliated Hospital of Dalian University (2023–2024). The model selected 16 predictors using LASSO and Boruta and was designed to integrate cross-sectional prediction with longitudinal dynamic assessment. A BRI-centered tool could improve risk stratification and early intervention for metabolic syndrome in midlife women, a group with high cardiometabolic burden.

Xi Y, Sun Q, Han Y et al. · Annals of medicine · (2026) · View on PubMed ↗

Association of inflammation with sex hormones and vitamin D in women: Findings from NHANES (2021-2023).

Using NHANES 2021–2023 data, this cross-sectional analysis examined associations between systemic inflammation (high-sensitivity C-reactive protein, hs-CRP) and sex hormones and vitamin D in 3,179 U.S. women aged 18–80 years. Women in the highest hs-CRP quartile had higher age and body weight, and multivariable linear regression assessed independent relationships between hs-CRP and endocrine biomarkers after confounder adjustment. These findings link inflammation with endocrine and vitamin D status in women, supporting inflammation-informed approaches to cardiometabolic and endocrine risk.

Abu-Zaid A, Baradwan S, Adly HM et al. · Scottish medical journal · (2026) · View on PubMed ↗

MASLD, diabetes and PMOS across the female life stages.

This article examined how metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes intersect across female life stages in the context of polyendocrine metabolic ovarian syndrome (PMOS, formerly PCOS). It reports mechanistic links in which PMOS-associated hyperandrogenism, insulin resistance, and chronic inflammation drive hepatic lipogenic gene programs and stellate-cell activation via androgen receptor signaling. The work highlights PMOS as a clinically important risk framework for earlier identification and prevention of MASLD and diabetes-related liver disease in women.

Stener-Victorin E, Carlsson S, Hagström H et al. · Diabetologia · (2026) · View on PubMed ↗ · Free PDF ↗

Evening circadian preference as a potential risk factor for cancer-depression comorbidity: a comprehensive analysis from population cohort to molecular insights.

Using prospective UK Biobank data (N=299,155), this study tested whether evening chronotype is associated with cancer–depression comorbidity across temporal transition pathways and used Mendelian randomization to probe shared causal biology. Evening chronotype was associated with increased risk of developing cancer–depression comorbidity, and molecular analyses suggested overlapping biological pathways that could link circadian preference to both conditions. The findings implicate circadian factors as potential targets for prevention or early intervention in individuals at risk for combined cancer and depression.

Tang L, Du Y, Liu S et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

The myokine irisin ameliorates the secretory dysfunction of pancreatic β cells in experimental and human type 2 diabetes.

This study tested whether the myokine irisin improves pancreatic β-cell secretory dysfunction in experimental and human type 2 diabetes (T2D), using diabetic mice and ex vivo human pancreatic islets from T2D subjects. Irisin administration improved glycemic control by increasing islet insulin content and glucose-stimulated insulin secretion and markedly stimulated β-cell proliferation in diabetic mice, while in T2D human islets it restored insulin content and glucose-stimulated insulin secretion. The results suggest irisin or irisin-mimetic strategies could preserve β-cell functional mass and counter β-cell failure in T2D.

Marrano N, Borrelli A, Biondi G et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of Ultra-Processed Foods Consumption on Human Health Outcomes: An Umbrella Review of Systematic Reviews and Meta-Analyses.

The study conducted an umbrella review of systematic reviews and meta-analyses to summarize evidence linking ultra-processed foods (UPFs), defined by the NOVA classification, to human health outcomes. Across the available literature, it synthesized associations between UPF consumption and multiple adverse health endpoints while assessing the quality of included evidence. This consolidates the current state of evidence for UPF-related risk and can inform public health guidance and future causal research.

Rodriguez-Hilarion JA, Ramos-Castaneda JA, Duran Aguero S et al. · Nutrition reviews · (2026) · View on PubMed ↗

Diabetes-associated MYT1 and ST18 genes regulate human beta cell insulin secretion and survival via other diabetes risk genes.

The study investigated how diabetes-associated MYT1 and ST18 genes regulate human pancreatic beta cell insulin secretion and survival, focusing on their control of other diabetes risk genes. Using human beta-cell models with MYT1 or ST18 perturbation (details truncated in the abstract), it tested the hypothesis that these myelin transcription factors prevent beta cell failure by repressing stress-response overactivation under normal and obesity-related conditions. This links specific diabetes-risk genes (MYT1/ST18) to beta-cell functional resilience, supporting them as mechanistic targets for type 2 diabetes prevention or therapy.

Hu R, Hamilton N, Wang Y et al. · Diabetologia · (2026) · View on PubMed ↗ · Free PDF ↗

Integrated 24-Hour Time Use Patterns to Mediate Depression and Cardiovascular Disease Comorbidity: A Shared Lifestyle Pathway.

This study used NHANES 2005–2018 data to examine how integrated 24-hour time-use patterns (sleep, work, and physical activity) relate to depression and cardiovascular disease (CVD) outcomes in U.S. adults, including cross-sectional and prospective cohorts. The authors report that a shared lifestyle pathway—captured by a novel time-use optimization algorithm—mediates the association between depression and CVD comorbidity and risk. These findings support time-use–based behavioral targets as a clinically actionable mechanism linking depression to CVD risk.

Zuo SH, Wang RY, Zhuo Y et al. · Mayo Clinic proceedings · (2026) · View on PubMed ↗ · Free PDF ↗

Association of 14 triglyceride-glucose (TyG)-related indices with new-onset cardiovascular disease in middle-aged and older adults: evidence from the CHARLS and ELSA aging cohorts.

Using longitudinal data from the CHARLS and ELSA aging cohorts (n=5,028) of middle-aged and older adults, this study assessed whether baseline and cumulative average triglyceride-glucose (TyG) indices predict new-onset cardiovascular disease. Higher sustained TyG-related risk patterns were associated with different CVD incidence risks, and the study aimed to quantify the added value of cumulative exposure and develop a clinically usable risk stratification tool. These findings support TyG-based measures as accessible markers for cardiometabolic risk stratification and potentially for earlier CVD prevention.

Zhu ZL, Hu HF · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular disease & vascular risk (atherosclerosis, aortic stenosis, stroke, hypertension)

PROTAC-mediated PCSK9 degradation attenuates atherosclerosis and improves plaque composition via suppression of NF-κB/TNF-α pathway.

This preclinical study developed Cadd4, a PROTAC designed to selectively induce proteasomal degradation of PCSK9, and tested its anti-atherosclerotic effects in RAW264.7 monocyte-macrophage cells, MOVAS vascular smooth muscle cells, and HUVECs. Cadd4-mediated PCSK9 degradation attenuated atherosclerosis and improved plaque composition by suppressing the NF-κB/TNF-α inflammatory pathway, with evaluation of long-term feasibility and safety. A PCSK9-degrading PROTAC approach could represent a next-generation therapy for atherosclerosis beyond conventional PCSK9 inhibition.

Wang X, Liu Y, Zhang QP et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Epidemiological and bioinformatics analyses of air pollution and genetic susceptibility in aortic stenosis risk.

This study assessed whether long-term air pollution exposure is associated with incident aortic stenosis (AS) risk and whether genetic susceptibility modifies this relationship using UK Biobank data. It found that per standard deviation increase, PM2.5 (HR 1.60), PM10 (HR 1.37), NO2 (HR 1.37), and NOx (HR 1.36) were each associated with higher AS risk, with consistent results across multiple internal validation approaches. The significance lies in providing gene–environment interaction and network toxicology support for air pollution as a modifiable cardiovascular risk factor for AS.

Ma Y, Jiang Q, Zhang J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Migraine and Stroke Risk in Postmenopausal Women in the Women’s Health Initiative.

This cohort study assessed the association between baseline, physician-diagnosed migraine and incident stroke (ischemic or hemorrhagic) in postmenopausal women enrolled in the Women’s Health Initiative. Migraine history was evaluated as the primary exposure using multivariable Cox proportional hazards models, with exclusions for prior stroke and missing key covariates. The findings are significant for clarifying whether migraine confers stroke risk in postmenopausal women, informing long-term cardiovascular risk stratification beyond reproductive-age populations.

Madsen TE, Raker CA, Pavlovic JM et al. · Neurology · (2026) · 1 citations · View on PubMed ↗

P2Y12 inhibitor monotherapy after abbreviated dual antiplatelet therapy following percutaneous coronary intervention: a meta-analysis.

The study performed a systematic review and meta-analysis of randomized controlled trials in percutaneous coronary intervention (PCI) patients comparing different timings of aspirin discontinuation after abbreviated dual antiplatelet therapy (DAPT), with P2Y12 inhibitor monotherapy as the strategy of interest. It evaluated major adverse cardiovascular events (MACE) using pairwise random-effects and network meta-analyses to determine whether stopping aspirin earlier versus later changes outcomes compared with continued DAPT. The results are intended to refine antiplatelet de-escalation protocols by identifying the safest timing for aspirin discontinuation in PCI patients.

Spagnolo M, Imbesi A, Bordonaro CA et al. · European heart journal · (2026) · View on PubMed ↗

ACADM-mediated fatty acid β-oxidation pathway in atherosclerosis and abdominal aortic aneurysm.

The study examined the role of ACADM-mediated fatty acid β-oxidation in atherosclerosis (AS) and abdominal aortic aneurysm (AAA) by integrating lipidomics, multi-omics analyses, functional assays, and machine learning. It compared lipid metabolic differences across mouse models and human cohorts and then used multi-omics to infer disease-specific downstream mechanisms involving ACADM-related metabolic pathways. By distinguishing metabolic drivers between AS and AAA, the work suggests ACADM-centered β-oxidation dysregulation as a potential biomarker or therapeutic entry point for vascular disease subtypes.

Zhang H, Sun L, Xu T et al. · European heart journal · (2026) · View on PubMed ↗ · Free PDF ↗

Extracellular vesicles in atherosclerotic cardiovascular disease: mechanisms and therapeutic implications.

The study reviewed the mechanisms and therapeutic implications of extracellular vesicles (EVs) in atherosclerotic cardiovascular disease, focusing on EVs from endothelial cells, leukocytes, platelets, erythrocytes, and vascular smooth muscle cells (VSMCs). It summarized how EV cargo—such as pro-inflammatory proteins and microRNAs—can impair endothelial function, promote leukocyte adhesion, increase oxidative stress, and amplify monocyte recruitment, cytokine release, and thrombotic signaling. This synthesis highlights EVs as mechanistic drivers and potential therapeutic targets or biomarkers across stages of atherosclerosis.

Amabile N, Aikawa E, Dignat-George F et al. · European heart journal · (2026) · View on PubMed ↗

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Kidney disease & nephrology therapeutics (CKD, pruritus, kidney outcomes)

Chronic kidney disease in cirrhosis: a study of inpatients from a global perspective.

This global, prospective registry study enrolled non-electively admitted inpatients with cirrhosis from 127 sites worldwide to assess the prevalence of chronic kidney disease (CKD; GFR <60 mL/min/1.73 m2 for >3 months) and its prognostic impact. Patients with CKD (CKD+) had worse clinical outcomes than those without CKD (CKD-), establishing CKD as a common and high-risk comorbidity in hospitalized cirrhosis. Clinically, routine kidney function assessment in cirrhosis in diverse settings may improve risk stratification and guide management of patients at highest risk of poor prognosis.

Wong F, Adebayo D, George J et al. · Gut · (2026) · View on PubMed ↗

Clinical Features and Outcomes of Lean Metabolic Dysfunction Associated Steatotic Liver Disease with Increased Alcohol Intake.

This retrospective cohort study used the Veterans Analysis of Liver Disease (VALID) database to characterize clinical features and major liver outcomes (MALO) and all-cause mortality in patients with Metabolic Dysfunction Associated Steatotic Liver Disease with Increased Alcohol Intake (MetALD), stratifying by lean versus non-lean status (BMI <25 kg/m2; <23 kg/m2 in Asians). Lean MetALD patients had distinct clinical presentation and risk profiles compared with non-lean MetALD, with differences in subsequent liver outcomes and mortality. The results support more nuanced risk assessment of MetALD that accounts for body habitus rather than relying solely on obesity-based definitions.

John BV, Soon S, Singal A et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

Efficacy and safety of finerenone in patients with chronic kidney disease: an individual participant data pooled analysis (INFINITY).

This individual participant data pooled analysis (INFINITY) evaluated the efficacy and safety of finerenone, a non-steroidal mineralocorticoid receptor antagonist, across a spectrum of chronic kidney disease (CKD) etiologies and across levels of glycaemia, eGFR, and albuminuria. Finerenone showed kidney and cardiovascular benefits with an overall safety profile consistent across CKD subgroups, supporting its use beyond CKD due solely to type 2 diabetes. The analysis strengthens evidence for broad, stratified application of finerenone to slow CKD progression and reduce cardiorenal events.

Neuen BL, Heerspink HJL, Perkovic V et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Finerenone in Persons with Chronic Kidney Disease without Diabetes.

This randomized, placebo-controlled trial studied finerenone, a nonsteroidal mineralocorticoid receptor antagonist, in adults without diabetes who had chronic kidney disease (CKD) with albuminuria and were receiving a renin-angiotensin system inhibitor. Finerenone improved kidney and cardiovascular outcomes compared with placebo in this non-diabetic CKD population. The results extend the therapeutic benefit of mineralocorticoid receptor blockade beyond type 2 diabetes, informing CKD management for a broader patient group.

Heerspink HJL, Neuen BL, Agarwal R et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Obinutuzumab or Tacrolimus in Primary Membranous Nephropathy.

In a phase 3 randomized trial in adults with primary membranous nephropathy, investigators compared intravenous obinutuzumab (an anti-CD20 type II monoclonal antibody) versus oral tacrolimus. The primary endpoint was complete remission at week 104 (urinary protein-to-creatinine ratio ≤0.3 with stable eGFR), and the study evaluated complete and partial remission rates and safety through that time point. Clinically, the trial directly tests whether obinutuzumab can achieve remission with a different risk profile than tacrolimus in membranous nephropathy.

Fervenza FC, Hou FF, Hao CM et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Finerenone in Patients With Chronic Kidney Disease Due to Glomerular Diseases: A Randomized Clinical Trial.

This prespecified exploratory subgroup analysis of a phase 3 randomized, double-blind, placebo-controlled trial evaluated finerenone in patients with CKD due to investigator-reported glomerular diseases. The study assessed efficacy and safety of finerenone versus placebo in this glomerular-disease subgroup. The results are important because they test whether finerenone’s kidney-protective effects extend to CKD etiologies beyond diabetic kidney disease.

Neuen BL, Perkovic V, Agarwal R et al. · JAMA · (2026) · View on PubMed ↗

Gut microbiota and the kidney-gut-skin axis in chronic kidney disease-associated pruritus: mechanisms and therapeutic implications.

This article reviews mechanisms linking chronic kidney disease-associated pruritus (CKD-aP) to the kidney–gut–skin axis in patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD). It highlights gut microbiota dysbiosis, gut-derived uremic toxins, intestinal barrier impairment, systemic inflammation, neuro-opioid pathway abnormalities, and skin barrier damage as interacting drivers of itch. The proposed framework supports microbiome- and barrier-targeted therapeutic strategies to reduce CKD-aP burden and improve clinical outcomes.

Chen S, Liu J, Ni H et al. · Frontiers in cellular and infection microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Safety and Synergy of Finerenone and Empagliflozin in Lowering Blood Pressure.

This secondary analysis studied blood pressure (BP) effects and early BP response predictors for combination therapy with finerenone plus empagliflozin versus monotherapy in participants with chronic kidney disease and type 2 diabetes from the CONFIDENCE trial (n=800). The analysis assessed systolic BP changes across baseline SBP categories and evaluated whether early (day 30) SBP changes mediate urinary albumin-to-creatinine ratio reductions. The results support the safety and potential synergistic BP-lowering contribution of combined finerenone/empagliflozin in CKD-T2D populations.

Agarwal R, Correa-Rotter R, Navaneethan SD et al. · Hypertension (Dallas, Tex. : 1979) · (2026) · View on PubMed ↗ · Free PDF ↗

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Respiratory & pulmonary disease (ILD, lung inflammation, TB sequelae, allergic rhinitis)

The 2025 ATS/ERS update of the international multidisciplinary classification of the interstitial pneumonias: implications for the pathologist.

This article reviews the 2025 ATS/ERS update to the international multidisciplinary classification of interstitial pneumonias and discusses implications for pathologists, building on prior 2002 and 2013 consensus frameworks. The update incorporates advances in distinguishing idiopathic versus secondary disease, recognizes progressive pulmonary fibrosis (PPF), and reflects newer molecular pathology concepts. For clinical practice, the revised classification aims to improve diagnostic consistency and multidisciplinary decision-making in interstitial lung disease.

Nicholson AG, Cooper WA, Fabre A et al. · Histopathology · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and safety of acupuncture-related therapies in the treatment of allergic rhinitis: a systematic review and meta-analysis.

This systematic review and meta-analysis evaluates acupuncture-related therapies for allergic rhinitis (AR) in human participants, comparing acupuncture plus medication, acupuncture alone, and conventional medication. It aims to synthesize efficacy and safety evidence across prospective and clinical contexts to determine which intervention strategies provide the best benefit-risk profile. The findings are intended to guide evidence-based clinical recommendations for AR management using acupuncture as a complementary or standalone option.

Ma J, Peng M, Song YG et al. · Frontiers in medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Predicting failure of extubation and non-invasive respiratory support in critically ill patients: clinical complexity, limitations of traditional indices, and machine learning perspectives.

This study examines predictors of extubation failure and failure of non-invasive respiratory support in critically ill patients, focusing on how clinical complexity limits traditional bedside indices and how machine learning may improve prediction. It reports that conventional indices have limited predictive accuracy and poor generalizability across heterogeneous ICU settings, motivating ML-based approaches for earlier and more reliable escalation decisions. Improved prediction of non-invasive support failure could reduce delayed transitions to invasive mechanical ventilation and thereby improve outcomes.

Notaro S, Giurazza R, Imparato A et al. · Frontiers in medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Interventions to reduce the impact of post-tuberculosis lung disease: a scoping review of the literature.

This scoping review systematically mapped interventions delivered during or after tuberculosis treatment that might reduce the impact of post-tuberculosis lung disease (PTLD), using Joanna Briggs Institute methodology and searching Embase from inception to March 31, 2025. The review identified multiple intervention categories—including host-directed therapy, therapeutic drug monitoring, inhaled pharmacotherapy, and antimicrobials beyond TB—that could plausibly affect PTLD outcomes. By cataloging the evidence landscape, it highlights gaps and priorities for future studies to prevent or mitigate long-term morbidity after TB.

Byrne AL, Günther G, Tadyanemhandu C et al. · BMC pulmonary medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Hematologic malignancies & guidelines (CLL, myeloma, leukemia, TB/other infections as relevant)

Genome scale CRISPRi reveals both shared and strain-specific vulnerabilities in genetically diverse drug-resistant strains of Mycobacterium tuberculosis.

This genome-scale CRISPR interference (CRISPRi) study mapped shared and strain-specific vulnerabilities across genetically diverse drug-resistant Mycobacterium tuberculosis strains. The authors found that resistance genotypes create collateral effects that increase sensitivity to knockdowns in overlapping functional pathways, with many resistant strains showing heightened vulnerability to tRNA synthetase inhibition compared with the drug-sensitive parental strain. These results nominate tRNA synthetases and other collateral pathways as promising targets for developing therapies effective against drug-resistant TB.

Wang X, Jowsey WJ, Cheung CY et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

CD19/CD22 bivalent CAR T cells in children, adolescents and young adults with B-ALL: final phase 1 trial results.

This phase 1 trial evaluated bivalent CD19/CD22 BBζ CAR T cells in children, adolescents, and young adults aged 3–39 with relapsed/refractory B-cell acute lymphoblastic leukemia (B-ALL), reporting outcomes for patients treated at the recommended phase 2 dose (3×10^6 transduced CAR T cells/kg). In the final phase 1 cohort, the bivalent CAR T approach showed a tolerable safety profile with evidence of anti-leukemia efficacy despite prior limitations in CD22 recognition seen in earlier experience. These results support further development of multiantigen (CD19/CD22) CAR T strategies to reduce antigen-escape risk in pediatric/AYA B-ALL.

Silbert SK, Gava F, Yates B et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma: Mayo Clinic Systematic Management and Risk-Adapted Therapy for Lymphoid Malignancies (lySMART) Consensus Guidelines 2026.

This article presents the 2026 lySMART consensus guidelines for chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) management in adults, focusing on risk-adapted therapy using modern targeted agents. It emphasizes that frontline treatment has shifted from chemoimmunotherapy to Bruton tyrosine kinase inhibitors, BCL2 inhibitors, and anti-CD20 monoclonal antibodies, with regimen selection guided by genetic risk, comorbidities, and patient preferences. The guideline synthesis is significant for standardizing evidence-based, genetics-informed treatment pathways across CLL/SLL care.

Parikh SA, Hampel PJ, Roeker LE et al. · Mayo Clinic proceedings · (2026) · View on PubMed ↗

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Autoimmunity & inflammatory disease (RA-ILD, MG, VEXAS, autoimmune translation)

Rheumatoid arthritis-associated interstitial lung disease: screening, diagnosis, and treatment-an expert group consensus statement.

This expert group consensus statement synthesized evidence on screening, diagnosis, and treatment of rheumatoid arthritis-associated interstitial lung disease (RA-ILD) for clinicians managing patients with rheumatoid arthritis. It provides practical recommendations on who to screen, when to initiate therapy, and how to select treatment regimens in the absence of high-quality trial data. Scientifically and clinically, the consensus standardizes RA-ILD care pathways to reduce variability and improve outcomes in a common, morbid complication of rheumatoid arthritis.

Solomon JJ, Dieudé P, Matson SM et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.

This study investigated whether complement C3 inhibition can restore nicotinic acetylcholine receptor (nAChR) antibody-mediated muscle pathophysiology in human myasthenia gravis (MG), using human muscle cells and sera from acetylcholine receptor antibody seropositive (AChR+) MG patients. Live-cell real-time calcium imaging showed that complement C3 inhibition counteracts the functional disruption of α- and β-subunit nAChR-dependent calcium signaling caused by patient antibodies. Scientifically and potentially clinically, it supports complement C3 as a therapeutic target to mitigate antibody-driven neuromuscular dysfunction in AChR+ MG.

Huang YF, Bhandage AK, Fichtner ML et al. · EBioMedicine · (2026) · View on PubMed ↗

Cell-type- and state-resolved transcriptomics uncovers distinct T cell and monocyte dysregulation in multiple sclerosis.

The study performed cell-type- and state-resolved transcriptomics on peripheral immune cells from 167 patients with multiple sclerosis (MS) and 42 healthy participants, profiling 1,075 transcriptomes across six T cell and monocyte states. MS-associated transcriptional dysregulation was stronger in primary (unstimulated) immune cells than in in vitro–stimulated counterparts, and it highlighted shared and cell-type-specific gene/pathway changes with regulators such as ZBTB16 in T cells and monocytes. This provides a higher-resolution molecular map of immune dysfunction in MS that can guide mechanism-focused biomarker discovery and targeted interventions.

Roostaei T, Fujita M, Touil H et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Cell autonomous inflammation in VEXAS is mediated by cGAS-STING.

This preprint studied the mechanism of cell-autonomous inflammation in VEXAS, focusing on how somatic UBA1 hypomorphic activity in mature myeloid cells triggers intrinsic immune activation. Using multi-omic, biochemical, and cell biological analyses in model systems and patient-derived cells, the authors found that loss of cytoplasmic UBA1 activity convergently disrupts ER-associated degradation (ERAD) and mitochondrial homeostasis, with inflammation mediated by the cGAS–STING pathway. The results connect UBA1-driven cellular stress to innate immune signaling and suggest cGAS–STING as a mechanistic therapeutic target in VEXAS.

Magaziner SJ, Collins JC, Miller B et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

Translating B-Cell and Plasma-Cell Targeting from Oncology to Autoimmunity: Modalities, Quantitative Bridging, and a Development Roadmap.

This review studied how B-cell and plasma-cell targeting strategies developed in oncology can be translated to autoimmune diseases, emphasizing quantitative bridging across disease contexts. The authors propose a development roadmap based on pathobiological archetypes—precursor-dependent states, compartment-dominant tissue inflammation, and long-lived plasma cell–weighted autoantibody production—to guide modality selection and trial design. The framework aims to improve rational development and dosing/endpoint translation for B-cell–axis therapies across oncology and autoimmunity.

Yuan M, Xu XS · Clinical pharmacology and therapeutics · (2026) · View on PubMed ↗

Raw defines a TIR-fold cADPR hydrolase cooperating with dSarm in development and axon degeneration.

The study identified and characterized Raw, a distinct TIR-domain protein family member, as a cADPR-specific hydrolase that cooperates with dSarm (SARM1/dSarm pathway) in development and axon degeneration. Biochemical and structural analyses showed Raw does not hydrolyze NAD but efficiently hydrolyzes cADPR, and both TIR domains are required for catalytic activity. These findings refine the molecular logic of axon degeneration by implicating cADPR metabolism via Raw alongside SARM1/dSarm signaling.

Chen F, Chen Z, Tan Y et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

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Developmental biology & congenital disease (Notch/phase separation, organogenesis, xenogeneic complementation)

Xenophagocytosis blockade enhances interspecies chimerism.

This study investigated xenogeneic donor cell engraftment in interspecies blastocyst complementation models by identifying an innate immune barrier termed xenophagocytosis in which host macrophages eliminate viable xenogeneic cells. Xenogeneic cells displayed elevated phosphatidylserine that was recognized by the phagocytic receptor Axl on host macrophages, and blocking xenophagocytosis via macrophage or Axl receptor genetic ablation (and other orthogonal strategies) enhanced interspecies chimerism. These mechanistic and intervention findings provide actionable targets (macrophage/Axl axis) to improve efficiency of generating human organs in livestock.

Wang S, Niizuma K, Liu DD et al. · Cell · (2026) · View on PubMed ↗

Deep-sea megafauna co-opts microbial energy metabolism genes to withstand ultra-long starvation.

Through morphological, physiological, and comparative genomic analyses of deep-sea isopods that survive ultra-long starvation, this study identified a dual adaptation involving reduced basal metabolic rate and a distended, food-retentive stomach. A key finding was an ancient horizontal gene transfer of the microbial energy metabolism-related gene ND1, followed by dosage enhancement via post-transfer duplication and very high, histone-regulated expression. This provides a concrete genetic mechanism for extreme starvation tolerance and illustrates how microbial genes can be repurposed to support long-term survival in deep-sea environments.

Yuan J, Zhang X, Li S et al. · Cell · (2026) · View on PubMed ↗

Aberrant Phase Separation of Endothelial MAML1 Causes Congenital Heart Disease by Suppressing Notch Activity.

This study investigated how an aberrant phase separation mechanism involving the Notch coactivator MAML1 contributes to congenital heart disease (CHD) using a patient-derived Q401K knock-in mouse model, an endocardium-specific Maml1 knockout mouse, and CRISPR-edited human heart organoids. The authors report that the Q401K mutation disrupts MAML1 phase separation and suppresses Notch activity, leading to CHD phenotypes. Scientifically, it links a specific MAML1 molecular defect to Notch signaling dysregulation, providing a mechanistic target for understanding CHD pathogenesis.

Tan Z, Qi Y, Chen Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗

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Genome engineering & gene editing technologies (CRISPR variants, prime editing, chemogenetics)

Replaying germinal center evolution on a quantified affinity landscape.

This work developed an experimental evolution framework to replay germinal center (GC) evolution by running over 100 monoclonal GC reactions and assigning immunoglobulin affinities to each cell using deep mutational scanning. The authors found that GC affinity maturation follows predictable outcomes driven by noisy but persistent selection on an affinity landscape, with exploration constrained by somatic hypermutation biases. The approach links measurable molecular fitness landscapes to GC dynamics, advancing quantitative models of how antibodies evolve toward higher affinity.

DeWitt WS, Vora AA, Araki T et al. · Cell · (2026) · View on PubMed ↗

The NTR/prodrug revolution: Tools for controlling cell loss and regeneration.

This eLife review studied the NTR/prodrug chemogenetic system as a tool for controlling cell loss and regeneration, with emphasis on nitroreductase (NTR) enzymes such as nfsB and prodrugs that become cytotoxic. It summarizes how the system enables precise spatiotemporal ablation in model organisms—especially zebrafish—by converting inert prodrugs into active toxic compounds. The review is significant for guiding future development of versatile ablation models for regenerative biology and developmental studies.

Kim GJ, Parsons M · eLife · (2026) · View on PubMed ↗ · Free PDF ↗

Fully Modified SpyCas9 Guide RNAs Enable Robust Genome Editing In Cells and In Vivo.

This study investigated whether fully chemically stabilized SpyCas9 guide RNAs (gRNAs) can improve genome editing in cells and in vivo by using iterative, structure-guided optimization. The authors introduced chemical modifications at each gRNA position, including 2’-amino-RNA, 4’-thio-RNA, and extended nucleic acid (exNA), to generate guide designs that maintain or enhance Cas9 activity while improving in vivo editing robustness. The results advance chemically modified CRISPR therapeutics by enabling more reliable genome editing across delivery contexts.

Vu KA, Zhang H, Amrani N et al. · bioRxiv : the preprint server for biology · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials, real-world evidence & clinical practice guidelines (ERAS, GLP-1 use, CLL/SLL, CSCC, perioperative, etc.)

Hyperbaric oxygen therapy improves clinical symptoms and functional capacity and modulates thalamic connectivity in ME/CFS: a prospective cohort study.

This prospective cohort study evaluated hyperbaric oxygen therapy (HBOT) in 30 patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) who received 40 HBOT sessions, assessing clinical outcomes at baseline, during treatment, and four weeks after. The primary endpoint was change in the physical functioning subscale of the SF-36, with secondary measures including core symptom severity and exercise capacity, alongside functional brain changes in thalamic connectivity. Demonstrating symptom and connectivity improvements would support HBOT as a feasible disease-modifying candidate for ME/CFS.

Kim L, Cammà G, Peters CK et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Oral small molecule GLP-1 receptor agonist aleniglipron in people with overweight or obesity: a randomized, double-blind, placebo-controlled phase 2b trial.

This randomized, double-blind, placebo-controlled phase 2b trial evaluated once-daily oral aleniglipron, a small-molecule GLP-1 receptor agonist, in 230 adults with overweight or obesity. At week 36, aleniglipron produced dose-dependent placebo-adjusted weight loss of −8.2% (45 mg), −9.8% (90 mg), and −11.3% (120 mg), meeting the primary endpoint with P<0.0001 versus placebo. These results support aleniglipron as an effective oral GLP-1RA candidate for obesity treatment and justify further phase 3 development.

Rosenstock J, Lingvay I, Ryan D et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Bridging the gap: estimates of undetected dementia in Brazil.

This study estimated the proportion of undetected dementia in Brazil by using Brazilian Unified Health System (SUS) prescription data for acetylcholinesterase inhibitors (AChEIs) as a proxy for recognized Alzheimer’s disease (AD). It found that dementia underdiagnosis varies by age, sex, and macro-economic region after adjusting for AD proportion among dementias, treatment coverage, and disease stage. The significance is that it quantifies the likely burden of missed dementia diagnoses in Brazil, informing public health planning and resource allocation for cognitive disorders.

Miguel ACC, Martins-Teixeira L, Aliberti MJR et al. · Age and ageing · (2026) · View on PubMed ↗

European consensus-based interdisciplinary guideline for invasive cutaneous squamous cell carcinoma. Part 1: Diagnostics and prevention - Update 2026.

This European consensus guideline update studied best practices for diagnostics and prevention in invasive cutaneous squamous cell carcinoma (CSCC) and synthesised evidence from multidisciplinary European expert societies. It provides updated, consensus-based recommendations for clinical management focused on diagnostic pathways and preventive strategies for invasive CSCC. The significance is that it standardizes care across Europe to improve early detection and reduce preventable disease burden in a high-incidence population.

Stratigos AJ, Dessinioti C, Garbe C et al. · European journal of cancer (Oxford, England : 1990) · (2026) · View on PubMed ↗

Enhanced recovery after surgery (ERAS®) society guidelines for gynecologic oncology: 2026 update.

This article updated the 2026 Enhanced Recovery After Surgery (ERAS®) society guidelines for perioperative care in gynecologic oncology surgery, based on evidence from publications searched in Embase and PubMed (2018–2025). The guideline recommendations for ERAS protocol items were graded using the GRADE framework and are stated to be based on the best available evidence across meta-analyses, randomized controlled trials, and large prospective cohorts. Clinically, it provides an evidence-graded, standardized perioperative care pathway intended to improve outcomes and reduce variability in gynecologic oncology surgical management.

Nelson G, Altman AD, Metcalfe A et al. · Gynecologic oncology · (2026) · View on PubMed ↗

Integrated Depression Care and Livelihood Interventions for Low-Income Women in Vietnam: Protocol for a Cluster Nonrandomized Controlled Trial (LIFE-DM).

This protocol describes a cluster nonrandomized controlled trial (LIFE-DM) to test integrated depression care and livelihood interventions for low-income women in Vietnam delivered through community health stations (CHSs). The trial is designed to evaluate the effectiveness of livelihood integration alongside depression care in a setting where CHSs typically lack trained mental health providers. If effective, the approach could provide a scalable, resource-constrained model for simultaneously addressing depression and economic hardship among economically disadvantaged women.

Ngo VK, Vu TT, Sobowale K et al. · JMIR research protocols · (2026) · View on PubMed ↗ · Free PDF ↗

Adjunctive Treatment with GLP-1 and Dual GLP-1/GIP Receptor Agonists for People with Type 1 Diabetes: Consensus Report and Practical Guidelines for Safe Use.

This consensus report and practical guideline addresses adjunctive use of GLP-1 receptor agonists and dual GLP-1/GIP receptor agonists in people with type 1 diabetes, focusing on safe implementation. It synthesizes evidence for incretin-based therapies (including agents such as exenatide as an early example) and provides recommendations for monitoring and risk mitigation. The guideline is significant for translating incretin therapy into safer, standardized practice in type 1 diabetes populations.

Garg SK, Akturk HK, Garg S et al. · Diabetes technology & therapeutics · (2026) · View on PubMed ↗

Scalable differentiation of human cardiac organoids from iPSCs generates cardiac tissues for cardiac cell therapy.

This study develops a scalable protocol to differentiate human induced pluripotent stem cells (iPSCs) into cardiac organoids (COs) for cardiac cell therapy, generating cardiac tissues with matured-like electrophysiology. It reports that COs containing cardiomyocytes, cardiac fibroblasts, and endothelial cells can be produced within 20 days with organized sarcomeres and potential gap junctions, and that bioreactor-assisted upscaling increases cell densities for regenerative medicine. The approach supports manufacturing-ready cardiac tissue constructs aimed at improving engraftment after transplantation into acutely infarcted myocardium.

Hamad S, Aksoy E, Kalil M et al. · Theranostics · (2026) · View on PubMed ↗ · Free PDF ↗

Rates of, Reasons for, and Reactions to Discontinuation of GLP-1 Receptor Agonists: A Narrative Review.

This narrative review studied real-world evidence on discontinuation, adherence, and persistence of GLP-1 receptor agonists (GLP-1RAs) in patients with type 2 diabetes and related conditions. The authors found inconsistencies in how discontinuation/adherence/persistence are defined and measured across studies, with few qualitative studies focused specifically on reasons for stopping GLP-1RAs. The review highlights methodological gaps that limit interpretation and supports more standardized, patient-centered research to improve long-term GLP-1RA use.

Heisey HD, Gregg LP, Verrico CD et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on June 07, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.