PubMed Trending Research Digest — July 08, 2026

Automated digest · 96 articles · 15 research areas · July 08, 2026

Overview

Across this week’s papers, a dominant theme is precision medicine powered by measurable biomarkers—especially imaging and “computable” pathology. In neovascular AMD, OCT angiography features and angiogenic biomarkers help predict faricimab durability and personalize dosing intervals. In oncology, AI models translate routine H&E slides into clinically actionable biomarker predictions (e.g., CLDN18.2 in gastric cancer), while radiogenomic and radiomics approaches aim to infer molecular status (e.g., EGFR mutations in lung cancer brain metastases; recurrence risk after BCG in bladder cancer) without additional invasive testing.

A second major thread is immune modulation and resistance control, spanning both mechanistic and translational work. Studies explore how innate immune pathways (cGAS–STING/ferroptosis, TLR9–B cell–CD2 signaling) can reshape anti-tumor immunity, while others dissect why therapies fail—such as tumor biomechanics limiting CAR-T killing, autophagy/ULK1-driven drug tolerance in EGFR-mutant NSCLC, and metabolic reprogramming that supports immune evasion (e.g., KLF5–TAZ–FASN–driven Treg differentiation). Cellular and epigenetic regulation of immune states (including exhausted CD8+ T cell fate via CTCF and chromatin hubs) further reinforces the idea that “state control” is a key lever for durable responses.

Finally, several studies connect inflammation, metabolism, and organ-level outcomes, often with an eye toward prevention and long-term risk. Work on renal fibrosis and kidney inflammation identifies new targets (e.g., IFN-λ signaling; Dpp3–Nrf2 immune activation thresholds), while cardiovascular papers highlight inflammatory axes and ferroptosis/redox control relevant to ischemia-reperfusion injury and calcification. In parallel, real-world and population studies on sleep, frailty/metabolic risk, and incretin therapies (GLP-1RA/tirzepatide) emphasize that systemic physiology—not just single disease pathways—shapes risk trajectories.

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Ophthalmic imaging & biomarkers in retinal disease

Association between angiogenic features and responsiveness to faricimab in treatment-naïve neovascular age-related macular degeneration with OCT angiography.

This prospective study evaluated OCT angiography (OCTA) morphological features of macular neovascularization in treatment-naïve neovascular age-related macular degeneration (nAMD) patients receiving faricimab, and related baseline angiogenic biomarkers to response after loading and fixed Q8W/Q12W/Q16W regimens. Patients classified as good responders (Q16W) showed imaging features associated with greater treatment durability compared with poor responders (Q8W/Q12W), with dosing interval determined by post-loading disease activity. These OCTA-derived angiogenic biomarkers could help personalize faricimab dosing intervals to improve long-term disease control in nAMD.

Sakai R, Ichioka A, Ideyama M et al. · Graefe’s archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · (2026) · View on PubMed ↗

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Switching/optimizing anti-VEGF therapy in retinal disease

Switching to aflibercept 8 mg in neovascular age-related macular degeneration: real-world outcomes according to switch indication.

This multicentre retrospective observational study analyzed 300 eyes with nAMD previously treated with anti-VEGF therapy that were switched to aflibercept 8 mg for non-response, suboptimal response, or durability-driven reasons. Visual and anatomical outcomes at 3 and 6 months after switching differed by switch indication, indicating that the reason for switching predicts subsequent response to aflibercept 8 mg. Clinically, this supports using the switch indication to set expectations and potentially guide treatment strategy after inadequate response to prior anti-VEGF agents.

Veritti D, Sarao V, Lupidi M et al. · Graefe’s archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · (2026) · View on PubMed ↗ · Free PDF ↗

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Renal fibrosis & kidney inflammation mechanisms

WTAP Deficiency Promotes Podocyte PANoptosis and FSGS via SPP1 Signaling.

This study investigated the RNA methylation regulator WTAP (Wilms’ tumor 1-associated protein) in human FSGS and an adriamycin-induced FSGS mouse model, focusing on podocyte-specific mechanisms. It found that WTAP deficiency promotes podocyte PANoptosis and focal segmental glomerulosclerosis via SPP1 (osteopontin) signaling, using constitutive and tamoxifen-inducible podocyte Wtap knockout models generated with Cre-loxP. Clinically, identifying the WTAP–SPP1 axis as a driver of podocyte PANoptosis highlights a potential molecular target to slow or prevent progression of FSGS.

Lu Y, Li P, Liu Y et al. · Circulation research · (2026) · View on PubMed ↗ · Free PDF ↗

Sirtuin 1 deficiency mediates chronic kidney disease-induced inflammaging cardiovascular calcification.

This integrative study investigated how Sirtuin 1 (SIRT1) deficiency contributes to chronic kidney disease (CKD)-induced inflammaging and cardiovascular calcification, focusing on calcific aortic valve disease (CAVD). Using UK Biobank population analyses, single-cell RNA sequencing of human aortic valves, genetic inference, and functional experiments, the authors identified SIRT1 downregulation and NLRP3 pathway activation specifically in myofibroblast valve interstitial cells (VICs), linking CKD to senescence and osteogenic programs. The work is important because it identifies SIRT1/NLRP3 axis mechanisms that could be targeted to prevent or treat CKD-associated aortic valve calcification.

Xu L, Zheng Y, Liu M et al. · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression.

This study used a neonatal mouse model of Salmonella enterica serovar Typhimurium infection to define how the bacterial effector SopB modulates host mucosal inflammation. SopB suppresses early epithelial cytokine release by preventing ADAM17 activation and membrane translocation (reducing membrane-bound TNFα release) and by reducing IL-18 secretion via mTOR-controlled secretory autophagy. These findings identify SopB–ADAM17/mTOR–autophagy signaling as a mechanism by which Salmonella delays disease progression and prolongs host survival, informing potential anti-virulence strategies.

Diab N, Yong CH, Stange EL et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Dipeptidyl peptidase 3 sets the threshold for immune activation and survival during experimental bacterial infection.

This study investigated dipeptidyl peptidase 3 (Dpp3) in vivo using Dpp3 knockout mice during experimental bacterial infection with Klebsiella pneumoniae. Dpp3 deficiency increased resistance, with early divergence in bacterial burden, improved survival, preserved tissue architecture, and reduced systemic inflammation, and adoptive transfer showed the protection was cell-intrinsic. Mechanistically, Dpp3 loss impaired inducible Nrf2 stabilization, linking Dpp3 to immune activation threshold control and survival during infection.

Facoetti A, Lambroia L, Fontana E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Declining but persistent hepatocellular cancer risk beyond 10 years of entecavir or tenofovir in chronic hepatitis B: Results of the PAGE-B cohort.

This study analyzed long-term hepatocellular carcinoma (HCC) incidence and predictors in 1644 Caucasian patients with chronic hepatitis B treated with the high-genetic-barrier nucleos(t)ide analogues entecavir or tenofovir, with 903 followed beyond 10 years (PAGE-B cohort). HCC risk persisted beyond year 10, with reported 10- and 15-year cumulative incidences of 10.9% and (truncated in the abstract) indicating ongoing risk despite long-term viral suppression. These findings support continued HCC surveillance in CHB patients even after a decade of entecavir/tenofovir therapy, informing long-term risk stratification and follow-up strategies.

Papatheodoridis GV, Dalekos G, Idilman R et al. · Journal of hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

The landscape of serum autoantibodies in lupus nephritis.

This review summarized evidence on serum autoantibodies in lupus nephritis (LN) using data from the Italian collaborative ZEUS study, assessing SLE/LN–related markers at onset of renal symptoms (T0) and after 12 months (T12). It focused on autoantibodies linked to renal pathology (including anti-dsDNA, anti-Histone 2A/3, anti-C1q, anti-ENO1, anti-ANXA1, and anti-SOD2 IgG2) alongside factors related to NETs and dsDNA degradation, with clustering analyses based on selected serum parameters (truncated). The work is significant for identifying antibody patterns that may help predict renal evolution and refine biomarker strategies in LN.

Bruschi M, Alberici F, Moroni G et al. · Autoimmunity reviews · (2026) · View on PubMed ↗

Interferon-λ drives renal fibrosis by coordinating epithelial-fibroblast crosstalk.

This study investigated the role of interferon-λ (IFN-λ) in renal fibrosis using human and mouse fibrotic kidney samples and mouse models with IFN-λ receptor deficiency or exogenous IFN-λ. IFN-λ signaling promoted fibrosis by acting preferentially on renal fibroblasts to drive activation and migration via ERK/JNK-dependent induction of TGF-β and downstream TGF-β–SMAD2/3 signaling. These findings identify IFN-λ as a therapeutic target to prevent or treat chronic kidney disease progression by interrupting fibroblast-driven fibrogenic signaling.

Zhou Y, Zhang Y, Zhu M et al. · The Journal of experimental medicine · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Infectious disease: malaria antigens, surveillance & resistance

Identification of genetic markers of quinine partial resistance in Plasmodium falciparum.

This genetic study used a human liver-chimaeric mouse model to perform a Plasmodium falciparum genetic cross between quinine-partially resistant and quinine-sensitive parasites and mapped resistance loci in 120 unique recombinant progeny. Quantitative trait locus analyses identified a polygenic quinine partial resistance architecture with major candidate segments on chromosomes 7 and 12, and gene-editing implicated PfCRT and a structurally similar putative transporter, DMT1, as primary chromosome 7 candidates. These results are clinically important because they pinpoint genetic determinants of quinine resistance that can inform surveillance and guide development of improved antimalarial strategies.

Kanai M, Mok S, Yeo T et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Pharmacokinetics and pharmacodynamics of a long-acting monoclonal antibody against malaria in African adults.

This study analyzed pharmacokinetics and pharmacodynamics of the long-acting anti-malaria monoclonal antibody CIS43LS (targeting the Plasmodium falciparum circumsporozoite protein) using serum from 348 Malian adults enrolled in a 6-month phase 2 trial. Using 3,777 serum samples, the authors fit a two-compartment, non-linear mixed-effects population PK model incorporating anti-drug antibodies and target-mediated drug disposition. These PK/PD insights support rational development and dosing of CIS43LS and related anti-malaria monoclonal antibodies to sustain protective efficacy.

Tran TM, Hu Z, Kayentao K et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

Plasmodium falciparum HSP90 inhibitors show divergent resistance despite a shared ATP-binding site.

This research examined resistance development in Plasmodium falciparum to two HSP90 inhibitors that share the same ATP-binding site: geldanamycin and AUY-922. It found divergent resistance despite the shared target—geldanamycin rapidly selected many mutations across its binding pocket (up to 10 mutations; ~22-fold resistance), whereas AUY-922 produced a single A41S mutation after much longer selection time with only ~2-fold resistance. Scientifically, the results indicate that ATP-site inhibitors can differ in resistance propensity and mutation localization, informing malaria drug design and resistance management.

Ko FH, Lukens AK, Laureano de Souza M et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

MGF100 but not MGF300 family is a potential multigene-deleted target for ASFV attenuation and live attenuated vaccine development.

This work tested whether deletion of African swine fever virus (ASFV) multigene families MGF100 or MGF300 from genotype II highly virulent strains could attenuate ASFV and support live attenuated vaccine development. It found that ASFV-Δ100 showed reduced growth kinetics, aberrant virus morphogenesis, and efficient attenuation, whereas ASFV-Δ300 retained virulence despite reduced growth kinetics in vitro. The significance is that MGF100 deletion is a promising genetic strategy for creating safer ASFV live attenuated vaccine candidates.

Dang W, Xu F, Du Y et al. · Virulence · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Immunodominant B-cell epitopes for precision surveillance of Plasmodium vivax malaria.

This study used computational immunology combined with empirical serology to identify immunodominant B-cell epitopes for precision surveillance of Plasmodium vivax malaria across multiple geographic settings. From 142 P. vivax proteins, six antigens (AMA1, CSP, DBP, MSP1, MSP9, and P12) were prioritized and 64 epitopes were screened by ELISA against sera from the China–Myanmar border, with multiplex immunoassay validation in Brazil, the Solomon Islands, and Papua New Guinea. The resulting epitope panel improves discrimination of asymptomatic infections, supporting more sensitive surveillance tools for P. vivax elimination efforts.

Zhao H, Zhu Y, Yin J et al. · Emerging microbes & infections · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmunity: immune tolerance & immunotherapy platforms

Autoantigen mRNA-LNP Vaccination Drives Therapeutic Efficacy in Preclinical Models for Autoimmunity.

This preclinical study tested whether mRNA lipid nanoparticle (mRNA-LNP) vaccines encoding disease-relevant autoantigens can induce therapeutic, antigen-specific immune tolerance in autoimmune models. In experimental autoimmune encephalomyelitis (EAE) and a type 1 diabetes (T1D) adoptive transfer model, MOG27-63 mRNA-loaded LNPs delivered systemically or intramuscularly attenuated disease severity and provided antigen-specific protection despite eliciting strong effector responses. These results suggest that immunostimulatory mRNA-LNP platforms can be repurposed for durable, antigen-targeted therapy in autoimmunity.

Baeten P, Beets K, Schalley T et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroscience: synaptic plasticity, memory & neuroinflammation

Granzyme K CD8⁺ T cells with tissue-resident features promote intestinal inflammation in patients with Crohn’s disease.

This study characterized CD8+ T cell subsets in Crohn’s disease (CD) and assessed their contribution to intestinal inflammation using single-cell RNA sequencing and T cell receptor sequencing. In 15 CD patients, analysis of 41,699 CD8+ T cells identified granzyme K (GZMK+) CD8+ T cells enriched in intestinal tissues (contrasting with granzyme B (GZMB+) CD8+ cells enriched in blood), and spatial transcriptomics in inflamed tissue from two patients supported tissue-localized inflammatory programs. The findings are significant because they implicate GZMK+ tissue-resident-like CD8+ T cells as potential drivers of intestinal inflammation and potential targets for CD immunotherapy.

Lee Y, Kim TY, Kim Y et al. · Experimental & molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Key targets and mechanisms by which gut microbiota-derived metabolites regulate Alzheimer’s disease through the immune - inflammatory pathway: Based on network pharmacology and molecular docking.

This network pharmacology and molecular docking study explored how gut microbiota-derived metabolites may regulate Alzheimer’s disease via immune-inflammatory pathways. It identified 14 key overlapping targets between metabolite-associated and AD-related genes, including IL6, NFKB1, IL1B, PTGS2, TLR4, and PPARG, with PPI analysis highlighting hub genes such as IL6, NFKB1, IL1B, CXCL8, PPARG, FOS, and JUN. The findings generate testable hypotheses linking specific metabolite targets to neuroinflammation mechanisms in AD.

Miao L, Hou F, Li G · PloS one · (2026) · View on PubMed ↗ · Free PDF ↗

Fatty Acid Binding Protein 5 Mediates Astrocytic Pyroptosis and Neuroinflammation in Epilepsy via cGAS/STING Pathway.

This study investigated how fatty acid binding protein 5 (FABP5) regulates astrocytic pyroptosis and neuroinflammation in epilepsy through the cGAS/STING pathway, using temporal lobe epilepsy (TLE) patient-derived astrocytes, epileptic mice, and primary cells. It found that FABP5 was upregulated in astrocytes in epilepsy and that astrocytic Fabp5 deletion attenuated pyroptosis, neuronal loss, and seizure activity, with the cGAS/STING pathway implicated as a mechanistic mediator. The significance is that FABP5-coupled cGAS/STING signaling may represent a therapeutic target to reduce neuroinflammation and seizure progression.

Chen C, Zhao Y, Lian Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Prefrontal Transcranial Pulse Stimulation for Major Depressive Disorder: A Randomized Clinical Trial.

This double-blind, sham-controlled randomized clinical trial tested prefrontal transcranial pulse stimulation in patients with major depressive disorder (Hamilton Depression Rating Scale score ≥14) at Hong Kong Polytechnic University. The study found that transcranial pulse stimulation produced antidepressant effects compared with sham, indicating efficacy for major depressive disorder. If confirmed in broader populations, this technique could expand noninvasive neuromodulation options for depression with a potentially favorable tolerability profile.

Qin PP, Jin M, Kan RL et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Palmitoylation of PSD-95 Orchestrates Learning-Dependent Metaplasticity in the Amygdala and Fear Memory.

This study examined how palmitoylation regulates learning-dependent synaptic metaplasticity and fear memory in the amygdala, focusing on palmitate cycling on PSD-95. Conditioned fear learning impaired amygdalar metaplasticity (not hippocampal), and PSD-95 palmitoylation was required for fear memory expression by controlling PSD-95–dependent LTP-like mechanisms at lateral amygdala synapses. Mechanistically, targeting PSD-95 palmitoylation could represent a strategy to modulate pathological fear memory and related learning-dependent disorders.

Shen ZC, Weng YX, Xia ZX et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Musculoskeletal pain & exercise/rehab interventions

Impact of creatine supplementation alone or combined with exercise on inflammatory and clinical outcomes in chronic musculoskeletal pain treated in the rheumatological field: a systematic review.

This systematic review evaluated creatine supplementation alone or combined with exercise in people with chronic musculoskeletal pain managed in rheumatology settings. Across included studies, creatine was assessed for effects on pain, physical function/disability, quality of life, muscle strength, skeletal muscle mass, and inflammatory markers, but the abstract does not provide the pooled efficacy/safety results. Clinically, the review aims to clarify whether creatine could be a safe adjunct to improve musculoskeletal outcomes and modulate inflammation in rheumatology patients.

Salazar-Méndez J, Núñez-Cortés R, Salazar-Orellana C et al. · Nutrition (Burbank, Los Angeles County, Calif.) · (2026) · View on PubMed ↗

Ultrasound Muscle Thickness Is a Poor Index of Criterion Magnetic Resonance Imaging Measures of Resistance Training-Induced Muscle Growth.

This study compared group-level changes in ultrasound-measured quadriceps muscle thickness (ΔMTUS) with criterion magnetic resonance imaging (MRI) measures of resistance training-induced muscle growth (Δmaximum anatomical cross-sectional area [ΔACSAMRI] and Δvolume [ΔVOLMRI]) in healthy young males (n=39) after 15 weeks of lower-body resistance training. The key finding was that ultrasound muscle thickness was a poor index of MRI-derived muscle growth at the group level and showed weak relationships with ΔACSAMRI and ΔVOLMRI. The significance is that MRI should be preferred when precise quantification of resistance training hypertrophy is needed, while ultrasound may be limited for tracking true muscle growth.

Balshaw TG, Funnell MP, McDermott EJ et al. · Medicine and science in sports and exercise · (2026) · View on PubMed ↗

Aerobic Exercise and Subthreshold Depressive Symptoms in Adolescents: Secondary Analysis of a Randomized Clinical Trial.

This prespecified secondary analysis evaluated whether a 12-month aerobic exercise intervention in adolescents aged 12 to 17 years in China (from a multicenter, cluster randomized clinical trial) was associated with reduced subthreshold depressive symptoms and explored related neural mechanisms. Aerobic exercise was associated with lower subthreshold depressive symptoms compared with control, with findings suggesting exercise-linked changes in brain function relevant to mood regulation. These results support aerobic exercise as a potentially scalable, nonpharmacologic intervention during adolescence and motivate further work to clarify the neural pathways mediating symptom improvement.

Yan X, Shao R, Jin J et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

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Oncology: AI/pathology radiomics & predictive biomarkers

Radiogenomic modeling of EGFR mutation status in brain metastases from lung adenocarcinoma: a multicenter study with biological interpretability.

This multicenter radiogenomic study analyzed 1303 brain metastases from 421 lung adenocarcinoma (LUAD) patients to predict EGFR mutation status using radiomics and interpretable machine learning. A four-task adaptive LightGBM-based classification framework trained on 3435 radiomic features extracted from T1, T2, and contrast-enhanced T1 MRI achieved strong performance for distinguishing EGFR+ and specific sensitizing mutations (e.g., 19Del and L858R) with biological interpretability. The findings are significant because they support noninvasive, clinically actionable prediction of EGFR mutation status in LUAD patients with brain metastases to guide targeted therapy.

Deng F, Chu X, Shi W et al. · NPJ digital medicine · (2026) · View on PubMed ↗ · Free PDF ↗

A virulent bacterial signature is associated with the development of recurrence following colorectal cancer surgery.

This study analyzed perioperative gut microbiota in patients undergoing colorectal cancer surgery to determine whether a bacterial signature predicts postoperative recurrence. A distinct virulent bacterial signature present during the perioperative period was strongly associated with development of postoperative tumors/recurrence. The results suggest perioperative microbiome profiling could serve as a biomarker to stratify recurrence risk after colorectal cancer resection.

Roh M, Barat B, Gilbert JA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Artificial intelligence-based prediction of claudin 18.2 expression and immune phenotype from routine histology to guide treatment decisions in patients with gastric cancer.

This retrospective study developed and validated an AI model to predict claudin 18.2 (CLDN18.2) expression and immune phenotype from routine hematoxylin-and-eosin (H&E) histology in patients with gastric cancer. The key finding was that AI analysis of H&E slides can serve as a scalable alternative to CLDN18.2 immunohistochemistry (IHC) and can be integrated with AI-derived immune phenotyping to support treatment decision-making for CLDN18.2-targeted therapy such as zolbetuximab. Scientifically and clinically, this could reduce tissue requirements, cost, and turnaround time for biomarker stratification in gastric cancer.

Kim HD, Shin S, Hwang W et al. · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

Interpretable machine learning model of contrast-enhanced CT radiomics for predicting post-BCG recurrence in high-grade non-muscle-invasive bladder cancer.

This retrospective study developed an interpretable machine learning model using contrast-enhanced CT radiomics to predict 5-year post-BCG recurrence in high-grade non-muscle-invasive bladder cancer (NMIBC), using 136 patients from one institution and an external cohort of 51 patients. The model achieved improved recurrence risk prediction by quantifying tumor heterogeneity from CT features and provided interpretable outputs to support clinical use. This could enable noninvasive, individualized surveillance and risk stratification after BCG in high-grade NMIBC.

Zou XC, Yu ZJ, Yuan YY et al. · World journal of urology · (2026) · View on PubMed ↗

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Oncology: prognostic scores & real-world treatment outcomes

Real-world prognostic assessment of the HERO score in metastatic urothelial carcinoma treated with enfortumab vedotin (ARON-2EV study).

This multicenter retrospective real-world cohort study assessed the prognostic performance of the HERO score (based on hemoglobin level and neutrophil-to-lymphocyte ratio) in metastatic urothelial carcinoma patients treated with enfortumab vedotin (EV) after platinum-based chemotherapy and immune checkpoint inhibitors. The key finding was the observed association between HERO score risk categories and survival outcomes (overall survival and progression-free survival) in EV-treated patients. This supports use of the HERO score as a clinically accessible prognostic tool to better stratify outcomes for patients receiving EV.

Roviello G, Ciccimarra F, Urabe F et al. · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

TRADE: tolerability of adjuvant abemaciclib at 6 months after initial dose escalation in patients with early-stage HR-positive/HER2-negative breast cancer.

This preplanned analysis of the prospective TRADE trial evaluated tolerability and clinical outcomes of adjuvant abemaciclib at 6 months after initial dose escalation in patients with early-stage HR-positive/HER2-negative breast cancer. The key finding was that the study reported outcomes at 24 weeks following the earlier dose-escalation strategy designed to reach and maintain abemaciclib 150 mg twice daily, with toxicity concerns (especially diarrhea) informing tolerability. Clinically, it helps define how well patients sustain the target dose and what tolerability profile to expect during longer follow-up after escalation.

Schlam I, Trapani D, Kim SE et al. · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

Phenotype, Severity, and Therapy of Patients With LRP4 Antibody-Associated Myasthenia Gravis in the German Myasthenia Gravis Registry.

This analysis of the prospective longitudinal German Myasthenia Gravis registry characterized phenotype, severity, and treatment patterns in lipoprotein receptor-related protein 4 antibody (LRP4-Ab)-positive myasthenia gravis (MG) compared with other antibody-defined MG subgroups. The key finding was that LRP4-Ab-positive MG represents a distinct serologic subgroup with specific demographics, clinical features, and disease burden scores (e.g., MG-ADL and MG-QoL15r) relative to other antibodies. Scientifically and clinically, it improves understanding of this rare MG subtype and can inform prognosis and management decisions.

Preßler H, Stascheit F, Aigner A et al. · Neurology · (2026) · View on PubMed ↗

Identification of patients at risk for poor survival among those with normal skeletal muscle mass: a multicenter retrospective validation study in gastric cancer.

This multicenter retrospective validation study examined gastric cancer patients with normal skeletal muscle mass index (SMI) undergoing radical gastrectomy (pStage I–III) to identify an SMI cutoff that predicts overall survival. The study derived and validated an SMI threshold within the “normal SMI” range that stratified patients by survival risk despite baseline normal muscle mass. Clinically, this enables more precise prognostication after gastrectomy and may guide risk-adapted follow-up or supportive interventions.

Matsui R, Yamamoto K, Yukawa Y et al. · Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · (2026) · View on PubMed ↗ · Free PDF ↗

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Oncology: immunotherapy/chemoimmunotherapy strategies

Tumor-draining lymph nodes shape the tumor microenvironment through enrichment of tumor-reactive effector-exhausted CD8+ T cells.

This study used integrative multi-omics analyses to compare tumor-draining lymph nodes and tumor microenvironments between microsatellite instability (MSI) and microsatellite stability (MSS) colorectal cancers. The authors identified a distinct population of tumor-reactive effector-exhausted CD8+ T cells enriched in tumor-draining lymph nodes that differed between subtypes. These findings connect lymph node immune composition to subtype-specific anti-tumor immunity and may help explain differential responses to immune checkpoint blockade.

Kong D, Feng L, Sun Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Ivonescimab plus gemcitabine and cisplatin as first-line therapy for advanced biliary tract cancer: a multicenter, open-label phase 2 trial.

This multicenter, open-label phase 2 trial studied first-line treatment with the anti–PD-1/PD-L1–targeting bispecific antibody ivonescimab combined with gemcitabine and cisplatin in 30 treatment-naive patients with unresectable locally advanced or metastatic advanced biliary tract cancer (BTC). The key efficacy endpoint was investigator-assessed objective response rate (ORR) and safety, with pretreatment tumor specimens collected for biomarker analyses (details truncated in the abstract). If effective and tolerable, this regimen could expand first-line options for advanced BTC and enable biomarker-driven patient selection for ivonescimab-based chemoimmunotherapy.

Xu Q, Zhou S, Zhang C et al. · Journal of hepatology · (2026) · View on PubMed ↗

Mismatch repair deficiency or microsatellite instability in locally advanced rectal cancer patients treated with total neoadjuvant therapy.

This study evaluated the prognostic impact of mismatch repair deficiency (dMMR) or microsatellite instability-high (MSI-H) in locally advanced rectal cancer (LARC) patients treated with total neoadjuvant therapy (TNT), using real-world data from an international TNT rectal cancer cohort. It assessed pathological complete response (pCR/CR), event-free survival (EFS), and overall survival (OS) stratified by MMR/MS status, with the detailed results truncated in the abstract. The significance is clarifying whether dMMR/MSI-H status can guide prognosis and potentially treatment decisions in TNT-treated LARC patients.

Benhima N, Audisio A, Gallio C et al. · European journal of cancer (Oxford, England : 1990) · (2026) · View on PubMed ↗

Cisplatin-gemcitabine-durvalumab reintroduction in advanced biliary tract cancer: a multinational real-world analysis.

This multinational real-world analysis evaluated cisplatin-gemcitabine-durvalumab (CGD) reintroduction in advanced biliary tract cancer (BTC) patients who progressed during durvalumab maintenance. The key finding was the comparative assessment of overall survival and progression-free survival for patients receiving CGD reintroduction versus alternative platinum-based regimens (FOLFOX/XELOX) after maintenance progression. Scientifically and clinically, it addresses whether reintroducing platinum plus durvalumab can restore disease control in this post–chemoimmunotherapy setting.

Camera S, Vogel A, Rimini M et al. · ESMO open · (2026) · View on PubMed ↗ · Free PDF ↗

Polatuzumab Vedotin Plus Rituximab, Gemcitabine, and Oxaliplatin in Relapsed or Refractory Diffuse Large B-Cell Lymphoma: Results From the Phase III, Randomized POLARGO Trial.

This phase III POLARGO trial evaluated polatuzumab vedotin plus rituximab, gemcitabine, and oxaliplatin (Pola-R-GemOx) in transplant-ineligible relapsed or refractory diffuse large B-cell lymphoma (R/R DLBCL) patients. The study randomized patients 1:1 after a safety run-in to assess efficacy and safety of Pola-R-GemOx as an alternative to standard options in this high-risk population. If effective, this regimen could expand treatment choices for R/R DLBCL patients who cannot receive autologous stem cell transplant.

Matasar M, Li Z, Vassilakopoulos TP et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

TLR9 Agonists Potentiate Adoptive T Cell Therapy in Cancer through a B Cell-CD2 Costimulatory Axis.

This study tested how TLR9 agonists enhance adoptive CD8+ T cell therapy in cancer through a B cell–CD2 costimulatory axis, comparing multiple TLR agonists including class B CpG. The key finding was that TLR9-activated B cells improve CD8+ T cell effector differentiation, metabolic fitness, and antitumor control via CD2-dependent signaling, with class B CpG uniquely programming superior responses in both murine and human systems. These results identify a mechanistic route to optimize TLR9 agonist selection and improve ACT efficacy.

Ruffin AT, Toliopoulos V, Smith AS et al. · Cancer research · (2026) · View on PubMed ↗ · Free PDF ↗

The Chaos of Choice in Large B-cell Lymphoma: A Call to Harmonize First-line Trial Design.

This article discusses first-line treatment trial design for newly diagnosed large B-cell lymphoma (LBCL) patients as the therapeutic landscape shifts beyond CHOP to include antibody-drug conjugates, bispecific antibodies, targeted agents, and CAR T-cell therapies. It finds that current phase 3 trials use heterogeneous control arms, eligibility criteria, and endpoints without a harmonized framework for clinical decision-making. The significance is that standardizing first-line trial design could improve comparability across emerging LBCL therapies and accelerate evidence-based selection of optimal regimens.

Chihara D, Westin JR · Blood · (2026) · View on PubMed ↗

Durable Responses and Cystectomy Avoidance with IL-15 Receptor Agonist NAI plus BCG In BCG-Unresponsive NMIBC with Carcinoma In Situ +/- Papillary Disease.

This study reports long-term outcomes from the QUILT-3.032 trial in BCG-unresponsive non-muscle-invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) ± papillary disease treated with the IL-15 receptor agonist nogapendekin alfa inbakicept (NAI; ANKTIVA) plus intravesical BCG. The key finding is durable complete response (CR) with reduced need for cystectomy, with primary CR rate assessed over time and secondary endpoints including duration of CR, progression-free survival (PFS), overall survival (OS), and disease-specific survival (DSS). Clinically, this supports NAI+BCG as a potential bladder-sparing strategy for a high-risk, BCG-unresponsive NMIBC population.

Chang SS, Chamie K, Seabury CA et al. · The Journal of urology · (2026) · View on PubMed ↗ · Free PDF ↗

Abemaciclib plus endocrine therapy in chemotherapy-treated patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative metastatic breast cancer.

This multi-institutional prospective cohort study evaluated real-world efficacy and safety of abemaciclib plus endocrine therapy in chemotherapy-treated patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) metastatic breast cancer. The combination showed clinically meaningful outcomes with an acceptable safety profile in this previously chemotherapy-exposed population. These data support the use of abemaciclib-based endocrine therapy beyond standard first/second-line settings and help refine treatment selection in practice.

Narui K, Miyahara K, Uemura Y et al. · Breast cancer (Tokyo, Japan) · (2026) · View on PubMed ↗

Immune checkpoint inhibitors in advanced cholangiocarcinoma: a systematic review of efficacy, safety, and emerging biomarkers.

This systematic review synthesized evidence on immune checkpoint inhibitors (PD-1/PD-L1/CTLA-4 inhibitors) for advanced cholangiocarcinoma, focusing on efficacy, safety, and emerging biomarkers across studies published through December 31, 2024. Overall, the review reported that ICIs can produce antitumor activity in subsets of patients, while safety profiles and biomarker signals varied across trials. The synthesis clarifies the current role of ICIs in cholangiocarcinoma and highlights biomarker directions needed to improve patient selection.

Nisa FU, Ali M, Khan T et al. · Journal of the Egyptian National Cancer Institute · (2026) · View on PubMed ↗ · Free PDF ↗

Next-Generation Checkpoint Combinations: Optimizing PD-(L)1-Based Therapy Across the Advanced, Adjuvant, and Neoadjuvant Settings.

This narrative review summarized how next-generation checkpoint combinations optimize PD-(L)1-based therapy across advanced, adjuvant, and neoadjuvant settings, concentrating on renal cell carcinoma, urothelial (bladder) cancer, and non-small cell lung cancer. It highlighted evolving combination strategies designed to overcome primary and acquired resistance to PD-(L)1 inhibitors and discussed how evidence supports changing positioning across treatment phases. The review provides a practice-relevant framework for selecting and sequencing PD-(L)1 combinations as clinical trial data mature.

Petrelli F, Colombo Zefinetti L, D’Alessio A et al. · Current oncology reports · (2026) · View on PubMed ↗

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Oncology: targeted therapy, resistance & mechanistic oncology

TRPV-1-targeted Fe-phenolate network provokes apoptosis and ferroptosis to treat non-small cell lung cancer.

This preclinical cancer study developed a TRPV-1-targeted iron–phenolate nanoplatform (FeOLDA) that self-delivers intracellular iron (Fe3+) and the TRPV1 agonist N-oleoyldopamine (OLDA) to treat non-small cell lung cancer (NSCLC). The key finding is that FeOLDA triggers TRPV1-mediated Ca2+ overload and mitochondrial/ER stress to induce apoptosis while iron drives Fenton chemistry to deplete GPX4/GSH, elevate lipid peroxides, and induce ferroptosis. Scientifically and therapeutically, dual induction of apoptosis plus ferroptosis aims to overcome NSCLC’s inherent ferroptosis tolerance and improve anti-tumor efficacy.

Wang Z, Shao L, Wang C et al. · Biomaterials science · (2026) · View on PubMed ↗

Targeting lysosomes with a novel chloroquine derivative induces irreversible lysosomal damage and disrupts autophagosome and lysosome assembly in cancer.

This preclinical study developed lysostilbenes, a new class of chloroquine (CQ)-pharmacophore–stilbene hybrid lysosome-targeting agents, and tested their effects in pancreatic ductal adenocarcinoma (PDAC). The key finding is that the lead compound lysostilbene-4 causes irreversible lysosomal damage and disrupts autophagosome–lysosome assembly, overcoming limitations of CQ/HCQ that stem from transient activity and toxicity. Therapeutically, more durable lysosome disruption may improve PDAC treatment by blocking lysosome-dependent nutrient recycling and stress tolerance.

Chauhan N, Guha Majumdar A, Bhutia SK et al. · Autophagy · (2026) · View on PubMed ↗

KLF5-driven TAZ-FASN signaling reprograms fatty acid metabolism to support Treg differentiation in lung cancer.

The study examined how KLF5-driven TAZ–FASN signaling reprograms fatty acid metabolism to support regulatory T cell (Treg) differentiation in lung cancer using human lung cancer specimens, genetically modified lung cancer cell models, Treg differentiation assays, and mouse tumor models. The key finding was that KLF5 activates a TAZ–FASN axis that increases fatty acid availability/usage in a way that promotes Treg differentiation, thereby supporting lung tumor immune evasion. This mechanistic link suggests targeting the KLF5–TAZ–FASN metabolic pathway could both disrupt tumor lipid metabolism and reduce pro-tumor Treg formation in lung cancer.

Huang H, Chen J, Zhong P et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Prognostic impact of KMT2A-PTD in acute myeloid leukemia in the NGS era: a multicenter retrospective study.

This multicenter retrospective study evaluated the prognostic impact of KMT2A partial tandem duplication (KMT2A-PTD) and other KMT2A abnormalities in 585 patients with de novo acute myeloid leukemia (AML) diagnosed between 1991 and 2020 using bone marrow/peripheral blood samples analyzed in the NGS era. KMT2A-PTD (assessed by targeted polymerase chain reaction/NGS-based approaches) and co-occurring genetic alterations were associated with distinct clinical features and prognosis compared with other KMT2A abnormality categories. These findings support incorporating KMT2A-PTD into NGS-based risk stratification for AML to better predict outcomes and guide management.

Tokura T, Wakita S, Fukunaga K et al. · Annals of hematology · (2026) · View on PubMed ↗ · Free PDF ↗

Structural insights into the MLH1-FAN1 interaction reveal an uncharacterized binding interface on MLH1.

This study used structural biology and biochemical assays to define how the mismatch repair protein MLH1 interacts with the nuclease FAN1. Crystal structures showed the MLH1 C-terminal domain binds FAN1 peptides containing either the MIP or MIM motifs with comparable affinities, revealing a conserved FAN1-MIP recognition mechanism and an uncharacterized MLH1 binding interface termed the S3 site for FAN1-MIM engagement. Co-immunoprecipitation supported these interactions, providing a molecular framework for how MLH1–FAN1 complex formation regulates repeat expansion relevant to Huntington’s disease.

Chen Y, Hu H, Shang X et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

AI-guided CRISPR screening reveals therapeutic targets in psoriasis.

This study performed an AI-guided, genome-wide CRISPR knockout screen in primary human epidermal keratinocytes to identify regulators of surface IL-17 receptor A (IL17RA) relevant to psoriasis. Using experimental enrichment plus VirtualCRISPR (a language-model framework trained on functional genomics), the authors prioritized candidate regulators and validated two with minimal effects on keratinocyte viability. The approach and targets support development of topical small-molecule therapies that modulate the IL-17/IL-17RA axis by controlling IL17RA regulation in keratinocytes.

Zhao C, Shih M, Ahmed S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

The emerging Nexus of STING signaling and ferroptosis: from mechanisms to therapeutic opportunities.

This article is a mechanistic review synthesizing evidence for bidirectional crosstalk between the cGAS–STING innate immune pathway and ferroptosis. It details how STING signaling can promote ferroptosis through iron metabolism pathways (including NCOA4-mediated ferritinophagy) and how ferroptosis-related signals can feed back to modulate STING activity. By consolidating these mechanisms, the review highlights therapeutic opportunities for diseases where STING signaling and ferroptosis intersect.

Lin X, Wen Y, Lang J et al. · Cell death discovery · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting endoplasmic reticulum export disrupts metabolic resilience in multiple myeloma.

This study tested whether disrupting COPII-dependent endoplasmic reticulum (ER) export affects multiple myeloma (MM) cell survival by using MM cell lines and primary patient-derived cells with pharmacologic inhibition of ER export. Inhibiting ER export induced cell death in multiple MM models, and the effect depended on the secretory status of MM cells, with secretory MM cells showing accumulation of misfolded proteins. The results identify ER export as a vulnerability in MM’s biosynthetic proteostasis pathway, suggesting a therapeutic strategy beyond targeting only proteasomal degradation.

Horzum U, Oberacher H, Haun M et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

ULK1, a novel therapeutic target to delay drug tolerance to EGFR-TKIs in an EGFR-mutant non-small cell lung cancer model.

This preclinical study tested whether inhibiting ULK1, a key autophagy-initiating kinase, can delay the emergence of drug-tolerant persister (DTP) cells and drug tolerance to EGFR tyrosine kinase inhibitors (EGFR-TKIs) in an EGFR-mutant non-small cell lung cancer (NSCLC) model. The key finding is that ULK1 inhibition delays EGFR-TKI tolerance compared with approaches that broadly target autophagy (the abstract contrasts with chloroquine’s lysosomal, non-specific mechanism), though full experimental outcomes are truncated. This is significant because it identifies ULK1 as a more specific therapeutic target to overcome or delay resistance in EGFR-mutant NSCLC.

Morita A, Rai K, Kuribayashi T et al. · Lung cancer (Amsterdam, Netherlands) · (2026) · View on PubMed ↗

SEPTIN7 Enhances Tumorgenesis and Therapeutic Resistance in Hepatocellular Carcinoma by Promoting FGFR4 Stabilization and Recycling.

This study investigated how the small GTPase SEPTIN7 drives tumorigenesis and therapeutic resistance in hepatocellular carcinoma (HCC) by promoting FGFR4 stabilization and recycling. SEPTIN7 was upregulated in human HCC with high stemness scores and was required for HCC initiation/progression in mouse models, while its loss reduced cancer stem cell self-renewal and therapy resistance in HCC cell lines and patient-derived organoids. Mechanistically targeting the SEPTIN7–FGFR4 axis could therefore overcome resistance and reduce recurrence risk in HCC.

Sun T, Sun Q, Zhang X et al. · Cancer research · (2026) · View on PubMed ↗ · Free PDF ↗

Stress granules as RNA triage hubs suppress extracellular vesicle secretion under oxidative stress in cancer.

This PNAS study investigated how stress granules (SGs) regulate extracellular vesicle (EV) secretion under oxidative stress in cancer cells. Using a bioluminescent EV-reporter screen, the authors found that SGs selectively suppress CD63+ EV release and that the clinical compound YM155 rapidly inactivates FOXO3a, leading to delayed but sustained reduction of CD63+ EV secretion. This reveals an actionable stress-adaptation pathway that could be exploited to modulate tumor EV-mediated communication.

Dong Y, Yoshida T, Maeda M et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

ROS-Targeted Nanomotor Therapy in OA: Cartilage Protection and Pain Relief.

This preclinical study developed nanozyme-based Janus nanomotors loaded with metformin (MET) for ROS-targeted therapy in osteoarthritis (OA) to protect cartilage and relieve inflammatory pain. The key finding is that the nanomotors exploit elevated joint ROS as chemical fuel via intrinsic superoxide dismutase (SOD) and catalase (CAT) activities, enabling self-propelled deep penetration and improved therapeutic effects compared with conventional delivery. The significance is a targeted intra-articular strategy that may overcome rapid clearance and poor tissue penetration while reducing ROS-driven OA pathology.

Zheng M, Liu C, Xia Q et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Discovery of a Potent NAMPT-Targeting PROTAC for the Suppression of Triple-Negative Breast Cancer via Macrophage Reprogramming.

This study designed and characterized a NAMPT-targeting PROTAC (proteolysis-targeting chimera) using OT-82 as the warhead to suppress triple-negative breast cancer (TNBC) via macrophage reprogramming. The key finding is that compound A13 potently degraded NAMPT (DC50 ~9.31 nM in MDA-MB-231 and ~12.54 nM in 4T1 cells) and inhibited TNBC cell proliferation, migration, and invasion while modulating the tumor microenvironment by promoting tumor-associated macrophage reprogramming. The significance is that targeted NAMPT degradation may overcome limitations of existing NAMPT inhibitors and provide a dual tumor- and microenvironment-directed therapeutic approach for TNBC.

Song Y, Yang C, Li Q et al. · Journal of medicinal chemistry · (2026) · View on PubMed ↗

Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1-ALS Autopsy Tissue Donors.

This cross-sectional autopsy tissue case series studied intrathecally administered tofersen distribution and estimated SOD1 reduction in somatic motor system tissues from 8 deceased SOD1-ALS autopsy tissue donors across three US academic centers. Tofersen was detectable in central nervous system tissues, and the analysis provided the first human estimates of SOD1 knockdown in relevant motor system regions. These findings strengthen the translational evidence for tofersen’s mechanism of action and inform future dosing and biomarker development in SOD1-ALS.

Guise AJ, Sellon MT, Roemer SF et al. · JAMA neurology · (2026) · View on PubMed ↗

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Oncology: CAR T & cellular immunotherapy optimization

Concurrent administration of BCMA and GPRC5D chimeric antigen receptor (CAR) T cells in advanced multiple myeloma.

This phase I dose-escalation trial studied concurrent infusion of BCMA-directed CAR T cells (MCARH125) with or without GPRC5D-directed CAR T cells (MCARH109) in heavily pre-treated patients with relapsed or refractory multiple myeloma. The key finding reported is that the trial was designed to establish safety of concurrent administration across three dose levels (NCT05431608), with results pending completion in the provided abstract. Clinically, combining BCMA and GPRC5D CAR T targeting is intended to overcome heterogenous antigen expression in myeloma and improve depth/durability of responses while maintaining acceptable toxicity.

Mailankody S, Mitra S, Herrera K et al. · Blood · (2026) · View on PubMed ↗

Single Cell Analysis of the Tumor Microenvironment Landscape Across the Disease Spectrum of Multiple Myeloma.

This study integrated paired single-cell RNA sequencing with T-cell and B-cell receptor sequencing from bone marrow of 235 multiple myeloma patients spanning precursor to active disease states. It identified dynamic, reproducible tumor microenvironment “ecotypes” using non-negative factorization of immune cell-subset composition, revealing coordinated shifts in T-, NK-, B-, and myeloid cell abundance and functional states across disease progression. Scientifically, this single-cell atlas of TME evolution provides a framework for understanding immune dysregulation and therapeutic resistance and for stratifying patients by immune ecosystem.

Dang M, Moreno Rueda LY, Acevedo Calado MJ et al. · Blood · (2026) · View on PubMed ↗

CD4-directed nanoblades enable selective genome editing in CD4+ cells and HIV suppression in vitro and in vivo.

This study developed CD4-directed Nanoblades (CD4-NBs)—murine leukemia virus-like particles pseudotyped with anti-CD4 nanobodies—to deliver CRISPR-Cas9 ribonucleoproteins into CD4+ T cells for HIV suppression in vitro and in vivo. CD4-NBs selectively targeted CD4+ cells and enabled efficient gene disruption using dual-guide targeting of conserved HIV tat/rev/env sequences, resulting in HIV suppression in both experimental settings. The work is significant because it provides a cell-specific genome-editing delivery strategy that could help eradicate or functionally silence integrated HIV proviral DNA in long-lived CD4+ reservoirs.

Van Cleemput J, De Cock M, Verbeek R et al. · EMBO molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Identifying and reprogramming softness-driven cancer stem-like cells overcomes CAR-T cell resistance in solid tumours.

This study examined how mechanical softness in solid tumors drives cancer stem-like cell states that resist chimeric antigen receptor (CAR) T cell killing, and tested whether reprogramming these cells can overcome resistance. Cancer cells cultured on soft matrices showed reduced CAR-T cytotoxic sensitivity along with elevated extracellular ATP and sustained calcium activity, and the authors used a doxycycline-gated calcium-activated transcriptional “mechano-recorder” to identify softness-responsive cells and reprogram them to restore CAR-T susceptibility. The findings are significant because they connect tumor biomechanics to CAR-T resistance mechanisms and suggest a strategy to improve CAR-T efficacy in mechanically heterogeneous solid tumors.

Qu Y, Wang Y, Zhu L et al. · Nature biomedical engineering · (2026) · 1 citations · View on PubMed ↗

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Cardiovascular disease: cardioprotection, thromboinflammation & vascular biomarkers

Disrupted erythrocyte S1P-eNOS axis promotes hypoxia, hypertension and fibrosis in obstructive sleep apnoea-hypopnoea syndrome.

This cohort study examined red blood cell (RBC) oxygen off-loading capability and nitric oxide (NO) bioactivity in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) compared with matched controls. The key finding is that disruption of the RBC S1P–eNOS axis promotes hypoxia, hypertension, and fibrosis during OSAHS progression. These mechanistic insights suggest early RBC/NO-pathway biomarkers and potential targeted interventions to prevent cardiovascular and renal complications of OSAHS.

Fan Y, Chen C, Luo C et al. · European heart journal · (2026) · View on PubMed ↗

Mortality effect of albumin fluid resuscitation in adults with septic shock: a systematic review and dual frequentist-bayesian meta-analysis of randomised trials.

This systematic review and dual frequentist–Bayesian meta-analysis studied whether albumin-based fluid resuscitation versus crystalloid resuscitation affects all-cause mortality in adults with septic shock across randomized controlled trials. The key finding was the pooled mortality effect of albumin resuscitation (up to 90 days) compared with crystalloids, synthesized using random-effects models and frequentist–Bayesian methods. Clinically, the results inform whether albumin should be preferred over crystalloids for septic shock resuscitation to improve survival.

Mendes H, Wen HK, de Souza H et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

A comprehensive plasma-based approach to thromboinflammation in bladder cancer: integrating lipidomics, thrombin generation, and NETosis biomarkers.

This study investigated systemic thromboinflammation in bladder cancer by integrating plasma lipidomics with thrombin generation and NETosis biomarkers in 87 bladder cancer patients (NMIBC and MIBC) and 30 controls. The key finding was that specific plasma lipidomic profiles were associated with bladder cancer diagnosis, stage, and prognosis and correlated with thromboinflammatory mechanisms, particularly NETosis and thrombin generation. These findings suggest a plasma-based multi-omics biomarker strategy could improve risk stratification and mechanistic understanding of bladder cancer–associated inflammation.

Oto J, Herreros-Pomares A, Verger P et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

VCAM-1 as a biomarker of early cardiac phenotypic changes in Fabry disease.

This exploratory single-center cross-sectional study measured vascular cell adhesion molecule-1 (VCAM-1) as a biomarker of early cardiac phenotypic changes in Fabry disease in 14 genetically confirmed adults from a family carrying the GLA p.Arg363His variant, compared with 30 matched healthy controls. The key finding was that VCAM-1 levels differed in Fabry participants and were associated with early cardiac phenotypic changes relative to controls. Clinically, VCAM-1 could serve as an accessible endothelial activation biomarker to detect early cardiac involvement in Fabry disease.

Lino DODC, Meneses GC, de Almeida IM et al. · BMC cardiovascular disorders · (2026) · View on PubMed ↗ · Free PDF ↗

The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers.

This study investigated the role of the H3K4 methyltransferase KMT2D as a cofactor for the transcription factor GATA1 during human erythropoiesis using human erythroid precursors. Loss of KMT2D caused developmental arrest with impaired expression of many erythroid genes, and KMT2D colocalized with GATA1 on >1,000 erythroid enhancers where co-occupancy correlated with stronger transcriptional activity. The work establishes KMT2D as an essential GATA1 cofactor at erythroid enhancers, providing mechanistic insight relevant to disorders of erythroid differentiation.

Zhang J, Xin Y, Cheng L et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.

This study examined the role of Bclaf1 in heart failure by using human HFrEF myocardium samples and male murine pressure-overload models with cardiac-specific Bclaf1 overexpression, knockout, or AAV9-mediated knockdown. Bclaf1 was elevated in HFrEF and promoted pathological hypertrophy and systolic dysfunction, while Bclaf1 loss or knockdown attenuated these phenotypes. Mechanistically, Bclaf1 recruited the splicing factor Srsf2 to enhance Hand2 pre-mRNA splicing, linking Bclaf1–Srsf2 splicing control to pathological cardiac remodeling and potential RNA-splicing therapeutic targets.

Zhang Y, Gao H, Lu Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

MDH1 K298 succinylation stabilizes redox homeostasis to protect against cardiac ferroptosis in ischemia-reperfusion injury.

This study investigated how site-specific lysine succinylation of malate dehydrogenase 1 (MDH1) at lysine 298 (K298) affects redox homeostasis and protects against cardiac ferroptosis in a murine myocardial ischemia-reperfusion (I/R) injury model. The key finding is that MDH1 K298 succinylation stabilizes redox homeostasis, thereby reducing ferroptosis-related injury during I/R (full mechanistic details truncated in the abstract). This is clinically relevant because targeting MDH1 succinylation or its downstream redox/ferroptosis pathways could represent a strategy to limit myocardial damage after I/R.

Li H, Liu J, Ren J et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

Jianpi Huayu decoction alleviates hepatic fibrosis involving coordinated modulation of PPARα-mediated lipid metabolic reprogramming and the ROCK pathway.

This in vivo and in vitro study tested whether allicin protects against myocardial ischemia-reperfusion (MI/R) injury by inhibiting toll-like receptor 4 (TLR4) and disrupting the mitochondrial DNA (mtDNA)-driven inflammatory and pyroptotic pathway. The key finding was that allicin suppressed mtDNA-mediated inflammation and pyroptosis through interference with the TLR4–mtDNA axis in MI/R models. This mechanistic evidence supports TLR4–mtDNA signaling as a therapeutic target and positions allicin as a potential cardioprotective candidate.

Luo R, Lai Y, Zhang S et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Inhibition of toll-like receptor 4 by allicin suppresses mitochondrial DNA-mediated inflammation and pyroptosis to alleviate myocardial ischemia-reperfusion injury.

This study used an AI-assisted high-content screening approach with multiplexed mitochondrial morphology to identify natural compound combinations that counteract UV-induced skin photoaging. The key finding was that AI-guided screening could pinpoint mitochondrial-enhancing natural compounds and combinations with protective efficacy against photoaging phenotypes. Scientifically, it provides a scalable strategy to discover mitochondrial-targeting natural products for skin aging interventions.

Liang S, Wu S, Yin J et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Fluoropyrimidine Cardiotoxicity: Role of Uridine Triacetate and Pharmacogenomic Insights from a Case of 5-FU-Induced Cardiogenic Shock.

This review examined fluoropyrimidine (5-fluorouracil and capecitabine) cardiotoxicity and highlighted the role of uridine triacetate alongside pharmacogenomic considerations, illustrated by a case of 5-FU-induced cardiogenic shock. The key finding is that severe fluoropyrimidine cardiotoxicity can present as fulminant cardiogenic shock and that uridine triacetate is relevant to management, with pharmacogenomic factors informing risk and treatment decisions. Clinically, this synthesis supports earlier recognition and targeted intervention for life-threatening fluoropyrimidine cardiac events.

Filomia S, Del Buono MG, Saponara G et al. · Journal of cardiovascular pharmacology · (2026) · View on PubMed ↗

Harnessing Large-Scale Multi-Omics Data for Risk Prediction and Deep Phenotyping of Valvular Heart Diseases in the General Population.

This study used UK Biobank multi-omics data to build and validate risk prediction models for valvular heart disease (VHD) and subtypes (aortic stenosis [AVS], aortic regurgitation [AVR], mitral regurgitation [MVR]) in the general population. The key finding is that Cox models using key clinical factors performed best among baseline approaches (C-index ~0.75–0.81), and adding proteomic data improved performance further (all C-index >0.81), whereas genomic data did not add similar benefit. The significance is that proteomics-enhanced models may enable more accurate deep phenotyping and risk stratification for VHD in routine population screening.

Jiang Z, Liu Y, Song M et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Cardiac myocyte contractility, calcium dynamics, and morphology in Zucker diabetic fatty female and male rats - lacking data in this model of obesity and diabetes: A review.

This review examined cardiac myocyte contractility, calcium dynamics, and morphology in Zucker diabetic fatty (ZDF) rats of both sexes, emphasizing gaps in data for this obesity/diabetes model. It synthesized evidence that diabetic cardiomyopathy in ZDF rats involves sex-specific alterations in myocardial structure and calcium handling that contribute to impaired contractile function. The review identifies where preclinical measurements are missing and guides future experiments to better model sex differences relevant to human diabetic cardiomyopathy.

Zahradnikova A, Ijaz H, Cagalinec M · Endocrine regulations · (2026) · View on PubMed ↗ · Free PDF ↗

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Metabolic health & weight management (GLP-1/IR/frailty/sleep)

Joint association of Insulin resistance and frailty index with incident ASCVD and MACE in individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: a multi-cohort study.

This multi-cohort observational study assessed the joint association of insulin resistance (IR) and a frailty index (FI) with incident atherosclerotic cardiovascular disease (ASCVD) and major adverse cardiovascular events (MACE) in individuals with cardiovascular–kidney–metabolic (CKM) syndrome stages 0–3. Using data from UK Biobank (n=259,714) and CHARLS (n=2,632), it evaluated IR-related indices together with FI to determine whether combined risk is greater than either factor alone. Scientifically and clinically, the results aim to refine risk stratification for ASCVD/MACE in CKM populations by incorporating both metabolic dysfunction and frailty.

Huang Y, Xu Y, Gu W et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Circadian regulation of cardiovascular function: from physiology to clinical implications.

This review summarizes how circadian rhythms regulate cardiovascular function, linking molecular clock networks and clock-controlled gene regulation to systemic outcomes such as blood pressure, heart rate variability, endothelial function, and vascular tone. The key finding is that circadian disruption from aging, genetic predisposition, or lifestyle factors increases risk of cardiovascular diseases including hypertension, atherosclerosis, heart failure, and arrhythmias. Clinically, it supports the rationale for chronobiology-informed prevention and treatment strategies targeting circadian mechanisms.

Malhan D, Ministrini S, Lin JC et al. · Genome medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Association between glycolipid metabolism 7 factors (GLM7) and pregnancy loss in women aged 18-35 years: evidence from NHANES 2009-2018.

Using NHANES 2009–2018 data, this study assessed the association between the glycolipid metabolism 7 factors (GLM7) index and pregnancy loss (single and recurrent) in women aged 18–35 years. The key finding was that GLM7 levels were associated with pregnancy loss risk, with the direction and strength of association quantified across categories of no loss, single loss, and recurrent loss. Scientifically, it supports the idea that glycolipid metabolic dysregulation contributes to adverse pregnancy outcomes and may help identify at-risk young women.

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

Adherence to planetary health diet and breast cancer risk: insights from a large case-control study in a low-and middle-income country setting.

In a matched case-control study in Morocco (2,800 women: 1,400 incident breast cancer cases and 1,400 controls), this research evaluated whether adherence to the EAT-Lancet “planetary health diet” is associated with breast cancer risk. The key finding was the relationship between higher adherence to the planetary health diet pattern and breast cancer odds, quantified across adherence levels. Public-health significance lies in supporting (or refuting) dietary pattern–based prevention strategies in low- and middle-income country settings.

Lamchabbek N, Mane N, Mrah S et al. · BMC public health · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists for Weight Loss and Risk of Major Safety Outcomes: A Multicentre Cohort Study.

This multicentre cohort study used electronic health records from 13 South Korean hospitals (2018–2025) to evaluate safety outcomes after initiation of weight-loss semaglutide or liraglutide versus propensity score–matched non-initiators. The key finding was the estimated associations (via Cox models and meta-analysis of site-specific hazard ratios) between GLP-1 receptor agonist initiation and major safety outcomes in real-world practice. The results are important for clinicians weighing semaglutide or liraglutide for weight management by clarifying comparative safety risks.

Park J, Kim JH, Kim YS et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Cardiovascular Outcomes With Tirzepatide Versus GLP-1 Receptor Agonists in Overweight or Obesity: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis compared cardiovascular outcomes associated with tirzepatide versus GLP-1 receptor agonists in adults with overweight or obesity using randomized and observational studies reporting cardiovascular endpoints. The key finding was the pooled comparative cardiovascular effect of tirzepatide relative to GLP-1 RAs, synthesized from eight studies (including one randomized trial) using adjusted hazard ratios when available. This informs evidence-based selection of incretin-based therapies for patients where cardiovascular risk is a primary concern.

Silva JPMRJ, Nogueira BV, Sartori DL et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Neuroinflammation in neurodegenerative diseases: pathogenic pathways and emerging pharmacotherapeutic targets in Alzheimer’s and Parkinson’s disease.

This narrative review summarized how neuroinflammation drives pathogenic processes in Alzheimer’s disease and Parkinson’s disease, focusing on microglia/astrocyte activation in response to amyloid-β/tau and α-synuclein and the resulting cytokine signaling and blood–brain barrier disruption. The key finding was that chronic innate immune activation links misfolded protein pathology to synaptic dysfunction, neuronal loss, and clinical deterioration, highlighting multiple emerging pharmacotherapeutic targets. Scientifically, it frames neuroinflammation as a tractable therapeutic axis and guides development of anti-inflammatory or immunomodulatory strategies for AD and PD.

Kumar RR, Kamaljeet, Kosey S · Inflammopharmacology · (2026) · View on PubMed ↗

Prolonged Short Sleep and Its Effect on Body Weight and Composition : A Pooled Analysis of Randomized Trials.

This pooled analysis of two randomized crossover trials examined the causal effect of 6 weeks of sleep restriction (SR) of 1.5 hours per night on body weight and body composition in adults with elevated cardiometabolic risk and habitual sleep of at least 7 hours. The key finding was the relationship between prolonged short sleep from SR and changes in energy balance/weight regulation outcomes, including potential differences by gender and menopausal status (as assessed in the pooled design). Clinically, it helps clarify whether chronic mildly insufficient sleep contributes to weight gain risk in at-risk adults.

Zuraikat FM, Scaccia SE, Cochran JA et al. · Annals of internal medicine · (2026) · View on PubMed ↗

Cardiovascular Risk Reduction With GLP-1 RA Drugs.

This article reviewed evidence that GLP-1 receptor agonists (GLP-1 RAs) reduce cardiovascular risk beyond glucose lowering in cardiometabolic disease. The key finding is that GLP-1 signaling improves vascular and myocardial function through effects on endothelial function, inflammation and oxidative stress, and cardiac metabolic remodeling, supported by large randomized cardiovascular outcomes trials. Clinically, it reinforces GLP-1 RA use as a cardiovascular risk-reduction strategy in appropriate patient populations.

Pigeyre M, Gerstein HC · Circulation · (2026) · View on PubMed ↗

Alcohol-Related Liver Disease: A Review.

This JAMA review synthesized evidence on alcohol-related liver disease (ALD) in the general population, focusing on epidemiology, clinical spectrum (from steatosis to steatohepatitis and beyond), and management considerations. The key finding is that ALD remains a leading cause of liver morbidity and mortality, with risk thresholds tied to long-term daily alcohol intake (e.g., >20 g/day for women and >30 g/day for men) and a broad disease continuum. Scientifically and clinically, the review underscores the need for prevention, early recognition, and effective treatment pathways—including transplant considerations—given ALD’s rising mortality burden.

Krag A, Åberg F, Mellinger J et al. · JAMA · (2026) · View on PubMed ↗

Tamsulosin Deprescribing for Lower Urinary Tract Symptoms in Older Men: A Randomized Clinical Trial.

This double-blind, placebo-controlled N-of-1 multiple crossover randomized clinical trial evaluated whether N-of-1 deprescribing can identify older men (ages 55 to 80) receiving minimal benefit from chronic tamsulosin for lower urinary tract symptoms attributed to benign prostatic hyperplasia. Participants randomized to tamsulosin discontinuation strategies showed outcomes consistent with identifying subgroups who could safely stop with limited worsening of LUTS compared with continued therapy. The approach provides a personalized framework for deprescribing tamsulosin and reducing unnecessary medication exposure in older men.

Bauer SR, Kenfield SA, Oni-Orisan A et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

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Aging, epigenetics & multi-omics biomarker frameworks

Genomic Medicine Sweden: Advancing precision medicine at the national level.

This article describes the establishment and operational approach of Genomic Medicine Sweden (GMS), a national program launched in 2017 to implement genomics-based precision medicine across Sweden’s publicly funded healthcare system. The key finding is the program’s coordinated model linking seven university healthcare regions with national partners to accelerate clinical adoption of high-throughput sequencing for rare diseases, cancer, and infectious diseases. Strategically, GMS provides a blueprint for scaling precision medicine at national level, addressing infrastructure, governance, and translation into routine care.

Edsjö A, Lindstrand A, Baliakas P et al. · Journal of internal medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Tandem repeat polymorphisms are associated with brain structure: results of two large population-based studies.

This study evaluated whether non-pathogenic short tandem repeat (STR) polymorphisms are associated with brain structure across the adult lifespan in the general population using two large population-based cohorts and targeted deep sequencing. The key finding is that tandem repeat polymorphisms show measurable associations with brain imaging-derived phenotypes, contributing to the “missing heritability” not captured by standard GWAS. Scientifically, it expands genetic architecture of brain structure beyond SNPs to include STR variation, informing future genetic risk models for brain-related traits.

Mantey R, Hu J, Touhidinia M et al. · Genome medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative Data on Long-Term Efficacy of Biologics in Moderate-to-Severe AD: An Expert Perspective on Using Indirect Comparison Methodology.

This expert perspective discussed how to compare long-term efficacy of biologics in moderate-to-severe atopic dermatitis using indirect comparison methods (specifically matching-adjusted indirect comparisons, MAICs) because head-to-head trials are lacking. The key finding was methodological guidance that MAICs can use individual patient data from one trial to adjust to summary statistics from another, enabling more valid cross-trial efficacy comparisons. This is significant for clinicians and researchers seeking comparative effectiveness estimates across approved biologics when direct randomized comparisons are unavailable.

Augustin M, Hong HC, Torres T et al. · Dermatology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Using human 3D organoid models to gain mechanistic insight in motor neuron diseases.

This review summarized how human induced pluripotent stem cell (iPSC)-derived 3D organoid models can be used to dissect mechanistic, cell-autonomous and non-cell-autonomous processes in motor neuron diseases (MNDs). It highlights organoid approaches such as spinal cord organoids to study motor neuron–glia interactions and other disease-relevant phenotypes in a controlled 3D context. The scientific significance is that these organoid systems can accelerate mechanistic discovery and therapeutic testing by better modeling the multicellular pathology of MNDs.

Frizzi B, Barbosa Correia AM, Faravelli I et al. · Nature reviews. Neuroscience · (2026) · View on PubMed ↗

Exhausted CD8+ T cell fate is programmed by dynamic CTCF-mediated enhancer activation and invariant CTCF-imposed barriers.

This study investigated how exhausted CD8+ T cell (TEX) fate is programmed during chronic viral infection by CTCF-mediated enhancer activation and chromatin barriers. Using mechanistic perturbation and chromatin analyses, the authors showed that CTCF acquires de novo binding sites in early TEX cells to open chromatin and activate enhancers with looping, and that invariant CTCF binding imposes essential barriers; genetic ablation of CTCF reduced chromatin accessibility/interaction strength and impaired TEX proliferation, effector function, and bioenergetic mobilization. The work is significant because it identifies CTCF as a key regulator of the epigenetic program that governs TEX differentiation and function.

Hu W, Zhu S, Chen Q et al. · Nature immunology · (2026) · 2 citations · View on PubMed ↗

Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted CD8+ T cell fate.

This study mapped self-associating chromatin hubs in CD8+ T cells to determine how exhausted CD8+ T cell fates are specified early during chronic viral infection. The authors found that chromatin hub assembly coincided with induction of effector versus stemness gene programs and identified Id2 and Id3 as key determinants, with Id2 promoting CD8+ TEX_EFF specification by activating effector genes while suppressing exhaustion and stemness-associated genes. The findings are significant because they connect 3D genome organization to transcriptional control of exhausted T cell fate, offering potential targets to modulate exhaustion for improved antiviral or immunotherapeutic responses.

Hu W, Chen Q, Zhu S et al. · Nature immunology · (2026) · 2 citations · View on PubMed ↗

From organ age gaps to precision geromedicine: multi-omic and imaging frameworks for heterogeneous biological aging.

This Review synthesized how biological aging can be modeled using multi-omic, imaging, digital biomarker, and genetic epidemiology data within an organ-level framework, introducing the ORGAN-AGE interpretive approach. It argues that signals from plasma proteomics, metabolomics, DNA methylation, imaging, and genetics are often interpreted more strongly than the evidence permits, emphasizing what these measures can and cannot establish. The significance is improved rigor in precision geromedicine by clarifying causal vs correlational limits of multi-omic “biological age” models for heterogeneous aging.

Li QM, Ge XX, Wen TJ et al. · Ageing research reviews · (2026) · View on PubMed ↗

Mapping sarcopenia’s causal proteome reveals a leptin-driven inflammatory-mitochondrial axis for early prediction.

This study mapped the causal proteome of sarcopenia using multi-omics and Mendelian randomization (MR) to identify a blood-based signature for early prediction, leveraging muscle transcriptomes and UK Biobank GWAS data. It reports a leptin-driven inflammatory–mitochondrial axis as the causal pathway underlying sarcopenia and proposes an early predictive signature (details truncated in the abstract). The significance is that a causal, blood-based biomarker approach could enable earlier identification of individuals at risk for sarcopenia before measurable muscle decline.

Sun J, Yan M, Dan J et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

Inherited retinal degenerations: clinical phenotypes and emerging therapies.

This Lancet Review summarized inherited retinal degenerations by clinical phenotype and emerging therapies, emphasizing the genetic heterogeneity revealed by testing across hundreds of genes. It highlights novel treatment modalities including gene therapy, cell-based approaches, optogenetics, and implantable chip therapies (with clinical presentation and disease categories organized by primary retinal cell type affected). The significance is guiding clinicians on phenotype-based diagnosis and accelerating translation of gene- and device-based interventions for progressive vision loss.

Uyhazi KE, O’Neil EC, Aleman TS et al. · Lancet (London, England) · (2026) · View on PubMed ↗

A global response contributes to tissue size robustness upon local induction of apoptosis.

This Current Biology study examined how a global response contributes to tissue size robustness when apoptosis is induced locally, focusing on compensatory coupling between cell death and tissue growth. The key finding (abstract truncated) is that local induction of apoptosis triggers system-level responses that help maintain overall tissue size despite localized damage. This is significant for understanding fundamental mechanisms of tissue resilience and for informing strategies to modulate regeneration or tumor responses to cell death.

Staneva R, Sobczyk-Moran G, Levillayer F et al. · Current biology : CB · (2026) · View on PubMed ↗ · Free PDF ↗

Histone chaperone HIRA regulates adiponectin expression and obesity-associated adipose expansion by facilitating Pol II pause release.

This study examined the role of the histone chaperone HIRA in adipose tissue biology by using adipose tissue-specific Hira knockout mice under high-fat diet-induced obesity. HIRA was required for Adipoq (adiponectin) and lipid metabolism gene expression by binding promoters/enhancers and facilitating RNA polymerase II pause release, and its loss impaired insulin sensitivity and restrained adipose expansion. Scientifically, it links epigenomic transcriptional control to obesity-associated adipose dysfunction and identifies HIRA as a potential regulatory target.

Wan D, Lee JE, Park YK et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial transcriptomic mapping of postnatal mouse uterine development.

This study generated spatially resolved transcriptomic maps of postnatal mouse uterine development from day 3 to day 21 by combining high-resolution in situ transcriptomics with histology, proteomics, genetic models, and functional assays. The key finding was that the temporal emergence and spatial arrangement of major uterine cell types can be defined, including that endometrial glands arise from luminal epithelium through progressive transcriptional reprogramming. These spatial atlases and lineage insights provide a framework for understanding normal uterine development and for interpreting developmental or reproductive disorders.

Jamaluddin MFB, Syed SM, Mohammed R et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 08, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.