PubMed Trending Research Digest — July 30, 2026

A curated digest of 94 trending PubMed articles, automatically categorised and summarised across 27 research areas.

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Diabetes, metabolic stress, and diabetic complications Cardiovascular epidemiology and risk prediction Atherosclerosis and immune inflammation in cardiovascular disease Lipid biology and LDL-C burden Kidney disease, renal injury, and cardiorenal/reno-cardiac syndromes Neurodegeneration and neuroinflammation (AD/PD/ALS/MS) Parkinson’s disease biomarkers and DBS-informed psychiatry Epilepsy and cGAS–STING innate immune signaling Psychiatric disorders, suicidality, and trauma-related trajectories Pain mechanisms and chronic pain syndromes Sleep disorders and circadian biology Cancer immunotherapy mechanisms and biomarkers Cancer therapeutics and comparative effectiveness Genomics, sequencing, and molecular diagnostics/biomarkers Cell therapy, CAR-T, and immune effector toxicity Virology, infectious disease, and host-pathogen interactions Plant biology, microbiomes, and phytopathogen control Bioengineering methods and omics technologies Tissue models, organoids, and spatial/3D mapping Mechanobiology and mechanosensitive immune regulation Hematology and clonal hematopoiesis malignancies Musculoskeletal biology, osteoarthritis, and bone remodeling Reproductive biology and 3D genome architecture Aging, senescence, and mitochondrial quality control Dermatology therapeutics (psoriasis/eczema/alopecia) Gastroenterology (Crohn’s/UC/cirrhosis) and GI outcomes Oncology surgery, radiotherapy/locoregional strategies, and surveillance

Automated digest · 94 articles · 27 research areas · July 30, 2026

Overview

Across this week’s set of studies, a dominant theme is mechanism-driven precision: from metabolic and epigenetic control (e.g., carbonyl detoxification disrupting arginine/insulin signaling; fasting-linked nuclear PI3K-3 chromatin co-activation; MMA overload driving diabetic cardiac injury) to immune and inflammatory signaling pathways (cGAS–STING in drug-refractory epilepsy; DR3 TL1A-dependent NF-κB activation; sTREM2–HSP90β in atherosclerosis; FcγR tuning to overcome checkpoint resistance). Several papers also emphasize that “system-level” context matters—spatial transcriptomics in Crohn’s fissure-to-fistula progression and sepsis-associated AKI, and human lung TRM mapping showing durable mucosal immunity beyond histology or bulk measures.

On the clinical and translational side, multiple efforts aim to improve risk stratification and treatment selection using biomarkers and comparative frameworks. Examples include imaging/clinical symptom profiling to predict amyloid copathology in Parkinson’s, automated Ki67 plus molecular scoring for meningioma prognosis, ctDNA methylation-guided surveillance after colorectal cancer resection, and proteogenomic/cis-pQTL strategies to prioritize new ischemic heart disease targets beyond statins. In oncology, real-world and comparative effectiveness studies (e.g., surgery after response in biliary tract cancer; AR pathway inhibitor comparisons in mHSPC) complement mechanistic immunotherapy work (DDR–immunity synergy; FcγR blockade; CD3-bispecific quantitative systems pharmacology) to connect “who benefits” with “why it works.”

Finally, the digest highlights broad advances in methods and models that make biology more tractable and human-relevant: AI-enabled mass spectrometry proteomics workflows, sequencing-free spatial profiling via nanoneedle arrays, and human glioblastoma organoid–brain slice models capturing infiltration heterogeneity. Parallel progress in therapeutics spans difficult-to-treat conditions (difficult hypertension with baxdrostat; steroid-sparing dermatology with tapinarof and pathway-specific PsA choices; systemic alopecia areata with oral JAK inhibitors; weekly long-acting HIV regimens; and novel RNA-degrader approaches for MYC-driven myeloma). Together, these papers point toward an increasingly integrated pipeline—better measurement, better models, and better mechanistic targeting—to reduce disparities and improve outcomes across chronic and acute diseases.

Diabetes, metabolic stress, and diabetic complications

Mitochondrial metabolism and epigenetic crosstalk drive SASP.

This study examined how mitochondrial metabolism regulates the senescence-associated secretory phenotype (SASP) by integrating mitochondrial DNA-driven innate immune signaling with epigenetic control in senescent cells. It found that upregulation of the mitochondrial pyruvate–citrate–acetyl-CoA axis increases acetyl-CoA availability to drive histone acetylation at SASP genes, enabling robust SASP transcription, while mitochondrial DNA activates inflammatory transcription factors via innate immune signaling. The results are significant because they reveal acetyl-CoA–dependent epigenetic licensing as a second control layer for SASP execution, suggesting metabolic-epigenetic targets to modulate senescence-driven inflammation.

Martini H, Birch J, Marques FDM et al. · Nature · (2026) · View on PubMed ↗

Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.

This review studied autophagy mechanisms in metabolic dysfunction–associated steatotic liver disease (MASLD) and their relevance to disease progression toward cirrhosis and hepatocellular carcinoma (HCC). The key finding was that impaired intracellular quality control—particularly disrupted selective autophagy processes such as lipophagy and mitophagy—contributes to hepatic lipid accumulation, oxidative stress, and hepatocellular injury. This provides a metabolic and precision medicine rationale for targeting autophagy pathways in MASLD.

Cazzaniga A, Frigo S, Cherubini A et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗

Methylmalonate Overload Despite Glycemic Control Drives Diabetic Heart Damage.

This translational study investigated why diabetic heart damage occurs despite glycemic control by focusing on methylmalonic acid (MMA) accumulation in the diabetic heart and its relationship to cobalamin (Cbl) status. The key finding was that MMA overload drives diabetic cardiac injury even when serum Cbl is normal or high, supported by analyses of serum Cbl/MMA and cardiac biomarkers in 12,751 participants and mechanistic characterization of the MMA pathway (including Mmut-related biology). This suggests MMA metabolism as a therapeutic target to prevent diabetic heart failure beyond glucose lowering.

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

The study analyzed 3025 adults with non-alcoholic fatty liver disease (NAFLD) from NHANES 1999–2018 to test how joint social determinants of health (SDoH) relate to NAFLD mortality and whether phenotypic age acceleration mediates these effects. Using weighted Cox models, a quantile-based g-computation (Q-gcomp) mixture approach, and mediation analysis via weighted logistic regression, the authors found that SDoH mixture effects on NAFLD mortality were mediated by accelerated phenotypic age. These findings link modifiable social exposures to biological aging pathways, supporting risk stratification and intervention targets for NAFLD outcomes.

Huang X, Zhang X, Yu X et al. · GeroScience · (2026) · View on PubMed ↗

The accumulation of methylglyoxal and acrolein impairs arginine homeostasis causing hyperglycemia and renal abnormalities in male zebrafish.

This study used CRISPR-generated male zebrafish lacking glyoxalase 1 (glo1) and aldo-keto reductase 1A1A (akr1a1a) to test how reactive carbonyl detoxification affects arginine metabolism, insulin signaling, and diabetes phenotypes. Double deficiency caused methylglyoxal and acrolein accumulation, suppressed arginine metabolism and insulin signaling, and led to hyperglycemia (including postprandial hyperglycemia in adults) plus renal abnormalities such as glomerular basement membrane thickening and podocyte effacement. The findings link carbonyl-detoxifying enzyme failure to arginine homeostasis disruption and insulin impairment, providing mechanistic support for targeting carbonyl stress in diabetic kidney disease.

Li S, Li H, Zhang X et al. · Nature communications · (2026) · View on PubMed ↗

Cardiovascular epidemiology and risk prediction

Antithrombotic treatment for migraine in patients with patent foramen ovale: multicentre, randomised, active controlled, open label trial.

This multicentre, randomized, active-controlled open-label trial evaluated antithrombotic strategies for migraine prevention in 1000 Chinese adults aged 18–64 years with migraine and patent foramen ovale (PFO) confirmed by echocardiography. The key finding was the trial’s assessment of efficacy and safety of antithrombotic treatment compared with an active control under blinded outcome assessment and hierarchical hypothesis testing. Scientifically and clinically, it tests whether targeting the PFO-associated thromboembolic mechanism can reduce migraine burden and inform management of migraine in patients with PFO.

Li Z, Wang C, Tang Y et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

Associations of accelerometer-derived daily step counts with future health risks: A phenome-wide association study among over 60,000 UK adults.

This prospective, population-based cohort phenome-wide association study examined associations between accelerometer-derived daily step counts and the risk of more than 400 incident disease phenotypes in over 60,000 UK adults. The key finding was the identification of step-count–disease associations across a wide range of outcomes using wearable-measured physical activity exposure. Clinically, it supports using step targets as a practical counseling metric by mapping how daily steps relate to future disease risk beyond traditional moderate-to-vigorous activity measures.

Liu HY, Liu YY, Ge XX et al. · International journal of nursing studies · (2026) · View on PubMed ↗

Anesthetic-Electrophysiologic Interactions: How Sedatives Shape Cardiac Conduction and Arrhythmia Risk.

This review summarized mechanistic, experimental, and clinical evidence on how anesthetic and sedative agents alter cardiac conduction and arrhythmia risk by modulating ion-channel activity, autonomic tone, and myocardial excitability. It specifically contrasts electrophysiologic profiles of agents such as propofol, dexmedetomidine, volatile anesthetics, ketamine, opioids, benzodiazepines, barbiturates, etomidate, and local anesthetics through effects on sodium, calcium, potassium, and pacemaker currents. The synthesis supports improved perioperative arrhythmia risk assessment and safer selection of sedatives/anesthetics in electrophysiology and critical care settings.

Tran HH, Thu A, Fuertes A et al. · Cardiology in review · (2026) · View on PubMed ↗

Baseline versus cumulative cholesterol, high-density lipoprotein, and glucose index and stroke risk in individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: evidence from the CHARLS study.

Using CHARLS data, this analysis compared baseline versus cumulative exposure to the cholesterol, high-density lipoprotein, and glucose (CHG) index for incident stroke risk in adults across cardiovascular-kidney-metabolic (CKM) syndrome stages 0–3. The key finding is that cumulative CHG index exposure is more informative for stroke risk than single baseline measurements in this CKM spectrum. This is significant because it supports using longitudinal metabolic-lipid burden metrics to refine stroke prevention strategies in CKM populations.

Chen C, Yang X, Li C et al. · Cardiovascular diabetology. Endocrinology reports · (2026) · View on PubMed ↗

Effect of empagliflozin on copeptin levels in patients with recent acute coronary syndrome and newly detected dysglycaemia: a post-hoc analysis of the SOCOGAMI randomized controlled trial.

In a post-hoc analysis of the SOCOGAMI randomized controlled trial, this study assessed whether empagliflozin changes copeptin levels in 42 patients after acute coronary syndrome (ACS) with newly detected dysglycaemia (impaired glucose tolerance or newly diagnosed type 2 diabetes) and no heart failure. The key finding is that empagliflozin modulates copeptin (vasopressin surrogate) compared with placebo over the trial period in this high-risk dysglycaemia population. This is significant because it links SGLT2 inhibitor cardiometabolic effects to potential vasopressin/fluid-regulation pathways relevant to cardiovascular risk.

Fortin E, Melander O, Ferrannini G et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗

Can baxdrostat redefine blood pressure control in resistant and uncontrolled hypertension? a systematic review, meta-analysis, and trial sequential analysis.

This systematic review, meta-analysis, and trial sequential analysis evaluated randomized controlled trials of baxdrostat, a highly selective aldosterone synthase inhibitor, in patients with uncontrolled or resistant hypertension. The pooled analyses reported that baxdrostat significantly reduced seated systolic blood pressure (with efficacy and safety assessed using random-effects models, TSA, and GRADE). Clinically, the findings suggest baxdrostat may be a promising add-on option for difficult-to-control hypertension, while emphasizing the need to interpret results in light of trial quality and evidence certainty.

Khan BW, Yahya M, Khan HW et al. · Naunyn-Schmiedeberg’s archives of pharmacology · (2026) · View on PubMed ↗

Racial and ethnic disparities in the cause of death for clear cell renal cell carcinoma.

This analysis of SEER registry data (2000–2019) studied racial and ethnic disparities in cause-specific mortality among patients with clear cell renal cell carcinoma, focusing on Black, White, and American Indian/Alaska Native (AIAN) groups. Black patients had the highest 5-year cumulative incidence of death (22.4% vs 21.7% in Whites), and mortality disparities persisted despite overall mortality declines (e.g., Black vs White HR 1.15, 95% CI 1.09–1.22; AIAN vs White HR 1.25, 1.10–1.43), with cardiovascular-disease death disparities increasing over time. These results highlight that non-cancer factors—particularly cardiovascular mortality—contribute to persistent outcome gaps, informing equity-focused risk management and care delivery strategies.

Xie Y, Zhang Y, Li S et al. · Nature communications · (2026) · View on PubMed ↗

Atherosclerosis and immune inflammation in cardiovascular disease

Soluble TREM2 Drives Atherosclerosis via HSP90β-Dependent Myeloid Inflammation.

This study investigated how soluble TREM2 (sTREM2) contributes to atherosclerosis through myeloid inflammation, with emphasis on an HSP90β-dependent mechanism. The key finding was that sTREM2 promotes atherosclerotic progression by activating HSP90β-linked inflammatory pathways in myeloid cells, consistent with prior observations that TREM2 influences foam cell formation and that sTREM2 is elevated in atherosclerosis plasma. This identifies sTREM2–HSP90β signaling as a potential target for anti-inflammatory therapeutic intervention in atherosclerotic cardiovascular disease.

Guo X, Liu X, Yu J et al. · Circulation research · (2026) · View on PubMed ↗

Lipid biology and LDL-C burden

This Global Burden of Disease Study 2023 analysis quantified the global burden of ischemic heart disease and ischemic stroke attributable to elevated LDL-C (relative to 35–54 mg/dL) from 1990 to 2023. Elevated LDL-C–attributable burden was estimated across countries and regions and decomposed into contributions from population growth, aging, risk-deleted burden, and exposure changes. The results provide population-level evidence to prioritize LDL-C prevention and treatment strategies worldwide.

Sherrod CF, Fontana M, Gillmore JD et al. · JAMA cardiology · (2026) · View on PubMed ↗

Global Burden of Elevated LDL-C: Findings From the Global Burden of Disease Study 2023.

This study used Global Burden of Disease Study 2023 methods to estimate the worldwide, regional, and national burden of ischemic heart disease and ischemic stroke attributable to elevated LDL-C from 1990 to 2023. It quantified how trends in LDL-C–attributable outcomes were driven by factors including population growth, aging, risk-deleted burden, and exposure changes. These estimates help policymakers target LDL-C reduction interventions to reduce cardiovascular morbidity and premature death.

Razo C, DeCleene NK, Johnson CO et al. · JAMA · (2026) · View on PubMed ↗

Kidney disease, renal injury, and cardiorenal/reno-cardiac syndromes

Early Prediction of External Ventricular Drain Weaning Trial Outcome in Patients with SAH Based on ICP Pulse Morphological Similarity: A Single-Center Retrospective Cohort Analysis.

This retrospective cohort study evaluated whether intracranial pressure (ICP) pulse morphological similarity could predict early external ventricular drain (EVD) weaning trial outcomes in patients with nontraumatic subarachnoid hemorrhage (SAH). Patients whose ICP pulse morphology remained similar—reflecting comparable mean ICP under homeostatic conditions—were more likely to succeed with EVD weaning than those with acute ICP dynamic changes. The approach could improve dynamic, early bedside prediction of weaning failure and thereby optimize ICU management of SAH.

Dong K, Sadan O, Horton P et al. · Neurocritical care · (2026) · View on PubMed ↗

Acute cardio-renal and Reno-Cardiac syndromes in critical care.

This narrative review synthesized evidence on acute cardiorenal syndrome and reno-cardiac syndrome in critical care, focusing on ICU-relevant CRS types 1 and 3. It summarized how acute heart–kidney and kidney–heart interactions are defined, recognized, and managed, particularly when renal replacement therapy is required. The review is clinically significant because it consolidates current knowledge to support improved diagnosis and treatment strategies in high-mortality ICU scenarios.

Girombelli A, Longhitano Y, Vetrone F et al. · European journal of internal medicine · (2026) · View on PubMed ↗

Intracranial pressure physiology, monitoring and individualized management in the acute brain injured patient.

This review article examined intracranial pressure (ICP) physiology, monitoring methods, and individualized management strategies in acute brain injury patients, including traumatic brain injury and ischemic/hemorrhagic stroke. It emphasized that while invasive ICP monitoring is established, interpretation and clinical use remain controversial and require individualized decision-making. The synthesis supports more nuanced ICP-guided management to reduce secondary cerebral insults and improve outcomes.

Taccone FS, Arabi Y, Baggiani M et al. · Intensive care medicine · (2026) · View on PubMed ↗

Identification of pulmonary hypertension with pulmonary vascular surface volume ratio by non-contrast CT.

This retrospective, two-center study investigated whether pulmonary vascular surface volume ratio derived from non-contrast CT can identify pulmonary hypertension (PH) and distinguish group 1 (pulmonary arterial hypertension, PAH) from group 2 (PH due to left heart disease, PH-LHD). Across participants who underwent right heart catheterization (RHC) and chest CT, it evaluated radiomic-morphological features from non-contrast CT to relate imaging phenotypes to RHC-defined PH categories. The clinical significance is that a non-invasive CT-based metric could improve early PH detection and reduce reliance on invasive RHC, especially for differentiating PAH versus PH-LHD.

Yu Q, Zhao Y, Huang Y et al. · BMC cardiovascular disorders · (2026) · View on PubMed ↗

Neurodegeneration and neuroinflammation (AD/PD/ALS/MS)

Transaldolase 1 contributes to pentose phosphate pathway disruption and synaptic dysfunction in Alzheimer’s disease.

The study examined how transaldolase 1 (TALDO1) affects pentose phosphate pathway (PPP) flux and synaptic function in Alzheimer’s disease using temporal cortex synaptosomes from AD patients and controls. Proteomic pathway disruption linked TALDO1 to reduced PPP activity and downstream synaptic dysfunction. These findings suggest TALDO1/PPP dysregulation as a mechanistic contributor to AD pathogenesis and a potential metabolic target to restore neuronal energy and synaptic integrity.

Hu X, Yu Y, Luo H et al. · Translational neurodegeneration · (2026) · View on PubMed ↗

Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer’s disease.

This study examined mitochondrial accumulation and lysosomal dysfunction in an Alzheimer’s disease mouse model using APP/PSEN1/mt-Keima mitophagy reporter mice. It showed that AD model mice develop mitochondrial plaques—large accumulations of acidic and neutral mitochondria in neuronal processes—driven by abnormal mitochondrial buildup and delayed lysosomal recruitment, with incomplete mitophagy due to impaired lysosomal function. The findings provide in vivo mechanistic evidence linking defective lysosomal degradation to pathological mitochondrial structures in AD.

Dan X, Croteau DL, Liu W et al. · Nature neuroscience · (2026) · View on PubMed ↗

Disease Course After Anti-CD20 Discontinuation in Secondary Progressive Multiple Sclerosis-A Multicenter Long-Term Longitudinal Study.

This multicenter retrospective longitudinal study assessed disease course after anti-CD20 discontinuation in selected secondary progressive multiple sclerosis (SPMS) patients in Austria and Switzerland who received no subsequent disease-modifying therapy (DMT). Among patients with ≥2 anti-CD20 cycles and ≥36 months follow-up, the primary endpoint was time to first confirmed EDSS worsening (≥0.5-point increase), with secondary outcomes including relapses, MRI activity, and severe infections. The findings inform clinical risk–benefit considerations for stopping anti-CD20 therapy in SPMS patients who remain treatment-free.

Otto F, Kliushnikova D, Radlberger RF et al. · Annals of clinical and translational neurology · (2026) · View on PubMed ↗

Neuroinflammation in Alzheimer’s and Parkinson’s diseases: pathogenic mechanisms and therapeutic strategies.

This review synthesized evidence on neuroinflammation mechanisms and therapeutic strategies in Alzheimer’s disease (AD) and Parkinson’s disease (PD), focusing on triggers such as amyloid-β (Aβ), hyperphosphorylated tau, and α-synuclein and their effects on glial cells. It reports that these endogenous pathological proteins activate glia and sustain chronic neuroinflammation across disease stages, while noting that no therapy specifically targeting neuroinflammatory processes has proven effective. The work is significant because it consolidates mechanistic targets for future AD/PD treatments aimed at interrupting glia-driven inflammatory amplification.

Wang QQ, Sun QQ, Guo YS et al. · Translational neurodegeneration · (2026) · View on PubMed ↗

Parkinson’s disease biomarkers and DBS-informed psychiatry

Subthalamic spatio-spectral-connectivity of psychiatric symptoms in Parkinson’s disease.

This study mapped neural oscillatory signatures to psychiatric symptoms in Parkinson’s disease using resting-state subthalamic nucleus (STN) local field potentials (LFPs) and frontal EEG in 55 patients undergoing deep brain stimulation (DBS). It tested whether symptom-specific frequency-domain neural signatures and machine-learning classifiers differ by eyes-open versus eyes-closed states and whether symptom encoding is spatially segregated within the STN. The results advance biomarker development for treating PD psychiatric symptoms via DBS-informed, frequency- and location-specific targeting.

Wang L, Zhao Y, Huang P et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗

Greater Motor and Nonmotor Burden at Diagnosis Is Associated With Amyloid Copathology in Parkinson’s Disease.

This retrospective study examined newly diagnosed, drug-naive Parkinson’s disease patients who underwent amyloid-β (Aβ) imaging to determine which baseline motor and nonmotor symptom profiles predict Aβ copathology. Among 152 patients completing smell testing (Cross-Cultural Smell Identification Test), autonomic testing, neuropsychological assessment, and NPI-Q, greater baseline motor and nonmotor burden was associated with amyloid copathology. Clinically, these symptom burdens could help identify early PD patients likely to have Alzheimer-type amyloid pathology, supporting risk stratification and prognosis refinement.

Na HK, Sun Y, Park CW et al. · Movement disorders : official journal of the Movement Disorder Society · (2026) · View on PubMed ↗

Epilepsy and cGAS–STING innate immune signaling

cGAS-mediated type I IFN signaling contributes to disease progression in drug-refractory epilepsy.

This study assessed whether cyclic GMP-AMP synthase (cGAS)-mediated type I interferon (IFN) signaling contributes to disease progression in drug-refractory epilepsy (DRE) in human brain tissue and mouse models of Dravet syndrome. It found robust type I IFN signatures and activation of upstream cGAS–STING signaling in microglia from individuals with DRE, and in Dravet syndrome models, with microglial cGAS activated by DNA released from hyperexcitable neurons. These results are significant because they implicate the cGAS–STING axis as a mechanistic driver of DRE progression and a potential therapeutic target.

Huang Y, Fan L, Wong MY et al. · Nature neuroscience · (2026) · View on PubMed ↗

Prior Sexual Violence, PTSD Symptoms, and Recovery Trajectories After New Trauma.

This case-control study examined longitudinal PTSD symptom trajectories after a new trauma in survivors with and without prior sexual violence (SV), using a longitudinal cohort sample. Participants with earlier SV history showed different (worse) PTSD symptom recovery trajectories after subsequent trauma compared with those without SV history. The findings clarify how prior SV shapes later PTSD course, informing risk stratification and tailored prevention or early intervention after new trauma.

Mellen EJ, Poplin T, Jovanovic T et al. · JAMA psychiatry · (2026) · View on PubMed ↗

Oral Semaglutide for Alcohol Use Disorder: A Randomized Clinical Trial.

This phase 2 double-blind randomized clinical trial evaluated oral semaglutide versus placebo in treatment-seeking adults with alcohol use disorder (AUD), using a dosing regimen of 3 mg/day for 4 weeks then 7 mg/day for 4 weeks over 8 weeks. The primary outcome was laboratory-based alcohol cue-elicited craving at week 6, with secondary outcomes including heavy drinking days and drinks per day. The trial tests whether GLP-1 receptor agonism can reduce alcohol craving and consumption, potentially offering a novel pharmacologic option for AUD.

Schacht JP, Sakai JT, Raymond K et al. · The American journal of psychiatry · (2026) · View on PubMed ↗

Mendelian Randomization Analysis of the IL-1 Cytokine Family Proteins Identifies IL1RL1 as a Potential Causal Contributor to Traumatic Brain Injury Prognosis.

The study used two-sample Mendelian randomization (MR) with inverse-variance weighting (IVW) to test whether genetically predicted circulating IL-1 cytokine family protein levels causally influence traumatic brain injury (TBI) prognosis. It identified IL1RL1 as a potential causal contributor to TBI outcomes based on publicly available genome-wide association study summary statistics. This provides a genetic rationale for IL1RL1 as a therapeutic or prognostic target in TBI-related inflammatory pathways.

Bhak Y, Helmy A, Needham EJ et al. · Neurocritical care · (2026) · View on PubMed ↗

Suicide in neurodegenerative diseases: a systematic review.

This systematic review (PRISMA 2020-guided) synthesized evidence on the relationship between suicidality and neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). The key finding was that suicidality is variably associated with these conditions across study designs, with disease-specific and methodological heterogeneity limiting firm causal conclusions. Clinically, the review underscores the need for routine suicide risk assessment and targeted mental-health interventions in patients with neurodegenerative disorders.

Abidar S, Nhiri M, Bianchi V · Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · (2026) · View on PubMed ↗

Convergent neuroimmune signaling underlying rapid antidepressant response to ketamine and psychedelics.

This study investigated convergent neuroimmune signaling for rapid antidepressant response to ketamine and serotonergic psychedelics by integrating cerebrospinal fluid (CSF) proteomics from healthy volunteers given intravenous ketamine with transcriptomic analyses in induced pluripotent stem cell (iPSC)-derived models from participants with treatment-resistant depression (TRD) and healthy volunteers. It found shared downstream molecular mediators/biological signatures across ketamine (and its metabolite (2R,6R)-hydroxynorketamine) and psychedelics including LSD and psilocybin that track with rapid antidepressant response. The results suggest common neuroimmune pathways that could yield shared biomarkers and guide development of faster-acting antidepressant strategies beyond the distinct primary receptor targets.

Jones GH, Gilbert JR, Johnston JN et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Genetically informed dissection of multimodal brain aging and ten major psychiatric disorders.

This genetic study examined shared genetic architecture between brain age gap (BAG) phenotypes and ten major psychiatric disorders by integrating UK Biobank-derived multimodal BAG GWAS summary statistics with Psychiatric Genomics Consortium and FinnGen GWAS data for psychiatric disorders. It identified significant genetic correlations and loci contributing to the overlap between BAG and psychiatric disease risk, using multimodal cross-trait genetic analyses to dissect shared heritability. These findings improve understanding of how neurobiological aging-related imaging phenotypes relate to psychiatric genetics and may refine risk prediction and mechanistic hypotheses for multiple disorders.

Zhao Q, An Q, Cai W et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Pain mechanisms and chronic pain syndromes

Phase 2b Trial of a NaV1.8 Inhibitor for Acute Pain.

This phase 2b, double-blind, randomized, placebo-controlled trial evaluated the selective NaV1.8 inhibitor LTG-001 in patients with moderate-to-severe acute postoperative pain after abdominoplasty. The key finding was the dose-ranging efficacy and safety assessment of LTG-001 given as a 300 mg loading dose followed by 150 mg every 12 hours or a 450 mg loading dose followed by 300 mg every 12 hours versus placebo and active comparator (hydrocodone bitartrate–acetaminophen). Clinically, it tests whether targeting the peripheral pain-signaling sodium channel NaV1.8 can reduce postoperative pain and inform dosing for future analgesic development.

Singla N, Katz NP, Vaughn B et al. · The New England journal of medicine · (2026) · View on PubMed ↗

This narrative review synthesized evidence on shared mechanisms—especially central sensitization (CS) and pain spread—and the implications for treatment across migraine, migraine-related neck pain, and low back pain. It reports that converging neurophysiological and clinical findings support overlapping central pain processing features across these chronic pain conditions and discusses pharmacological and rehabilitation-based interventions targeting these mechanisms. The significance is that recognizing common central mechanisms may enable more unified, mechanism-informed treatment strategies across seemingly distinct pain syndromes.

Onan D, Kodounis M, Pellesi L et al. · Pain and therapy · (2026) · View on PubMed ↗

Sleep disorders and circadian biology

Current and Emerging Therapies for Pediatric Sleep Disorders: A Narrative Review.

This narrative review summarized current and emerging therapies for pediatric sleep disorders, focusing on obstructive sleep apnea (OSA), insomnia, narcolepsy, and sleep-related movement disorders. It highlighted that pediatric OSA (about 2–5% prevalence) is commonly managed with multimodal care with adenotonsillectomy as first-line treatment, while residual disease remains common. The review supports updated, condition-specific treatment approaches to improve neurodevelopmental and behavioral outcomes in children.

Estrada Chaverri L, DelRosso LM, Ceballos Fuentes FA · Neurology and therapy · (2026) · View on PubMed ↗

Evening Light-Emitting Diode Screen Exposure, Melanopsin-Mediated Circadian Disruption, and Optical Filtration for Sleep Hygiene: A Narrative Review in the Indian Context.

This narrative review studied how evening exposure to light-emitting diode (LED) screens affects melanopsin-mediated circadian disruption and sleep hygiene, focusing on the Indian context with high smartphone and digital screen use. The key finding was that evening LED screen light can blunt melatonin and delay circadian timing via intrinsically photosensitive retinal ganglion cells (ipRGCs), while actual risk depends on melanopic light dose reaching the retina rather than screen time alone. This supports practical sleep-hygiene recommendations tailored to high digital-screen environments.

Dubey SA, Elango N, Blessy Coelho L et al. · Cureus · (2026) · View on PubMed ↗

Cancer immunotherapy mechanisms and biomarkers

Functional Engineered Exosomes Loaded with Nanoenzymes Targeting the Proteasome and Inflammation for the Treatment of Rheumatoid Arthritis.

This preclinical study engineered mesenchymal stem cell–derived exosomes loaded with nanoenzymes to target the proteasome and inflammation for rheumatoid arthritis treatment. The key finding was that genetically engineered exosomes could home to inflammatory sites in the affected limb, modulate the local immune microenvironment, and provide SOD-like and CAT-like enzymatic activity to counter oxidative/inflammatory damage. This supports a targeted exosome–nanoenzyme therapeutic strategy for RA that may improve efficacy over conventional non-targeted exosomes.

Liu E, Shen C, Zhao Q et al. · Small (Weinheim an der Bergstrasse, Germany) · (2026) · View on PubMed ↗

Binding of death receptor 3 (DR3) to intracellular TRADD and TRAF2 is independent of its natural ligand, TL1A.

This mechanistic immunology study examined proximal death receptor 3 (DR3) signaling in TF-1 cells and primary human CD4+ T cells, testing whether adaptor recruitment depends on the natural ligand TL1A. The authors found that TRADD and TRAF2 associate with DR3 independently of TL1A stimulation, whereas TL1A was strictly required for NF-κB activation (including IκBα degradation and downstream ubiquitination). These findings refine the DR3 signaling model and support more targeted therapeutic strategies against TL1A–DR3–NF-κB inflammatory pathways.

Sun W, Johnson BG, Veerasubramanian PK et al. · Journal of immunology (Baltimore, Md. : 1950) · (2026) · View on PubMed ↗

Tailored FcγR blockade enhances immune checkpoint therapy and overcomes resistance.

This preclinical study tested tailored Fcγ receptor (FcγR) blockade to enhance immune checkpoint therapy and overcome resistance using mechanistically matched murine surrogate and human lead FcγR-blocking plus immune checkpoint-blocking antibodies, including clinical reagents such as ipilimumab. It found that selectively targeting FcγRIIB or blocking all FcγRs can improve anti-tumor efficacy and tolerability of immune checkpoint blockade in vivo and in vitro, including in resistant settings. The significance lies in providing a rational Fc-engineering strategy to augment checkpoint immunotherapy by modulating IgG/FcγR effector pathways.

Oldham RJ, Mårtensson L, Semmrich M et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗

A genome-wide CRISPR screen in human prostate cancer cells reveals drivers of macrophage-mediated cell killing and positions AR as a tumor-intrinsic immunomodulator.

The study performed a genome-wide CRISPR screen in human prostate cancer cells using a macrophage co-culture system to identify tumor-intrinsic genes required for macrophage-mediated killing. It identified androgen receptor (AR), PRKCD, and multiple NF-κB pathway components (IKBKB/IKBKG/CHUK) as key drivers, with mechanistic linkage showing AR and NF-κB directly induce PRKCD expression. This positions AR as a tumor-intrinsic immunomodulator and highlights actionable pathways that could be targeted to enhance innate immune clearance of prostate cancer.

Zaalberg A, Lacoste A, Minnee E et al. · Oncogene · (2026) · View on PubMed ↗

The genetic architecture of fibromyalgia across 2.5 million individuals.

This review article examined how the DNA damage response (DDR) intersects with cancer immunotherapy mechanisms. It reports that DDR-deficient tumors or tumors treated with DDR inhibitors can generate immunogenic signals—neoantigens that activate tumor-specific T cells and cytosolic DNA that triggers the cGAS–STING pathway to induce type I interferon and immune recruitment. The significance lies in explaining why DDR-targeting strategies can synergize with immunotherapies and suggesting biomarkers and combination approaches to improve patient responses.

Kerrebijn I, Bjornsdottir G, Arbabi K et al. · Nature medicine · (2026) · View on PubMed ↗

Cancer therapeutics and comparative effectiveness

A first-in-class RNA degrader reduces c-MYC expression and myeloma cell survival in preclinical models.

This preclinical study tested a first-in-class RNA degrader, a MYC-RiboTAC ribonuclease-targeting chimera, in multiple myeloma (MM) using RNaseL-dependent mechanisms across MM cell lines and a panel of primary patient MM samples. The key finding was that MYC-RiboTAC reduced MYC mRNA and MYC protein levels in an RNase L-dependent manner, thereby decreasing myeloma cell survival. This is significant because it provides a strategy to therapeutically degrade MYC mRNA (rather than the intrinsically disordered MYC protein), supporting RiboTACs as a potential platform for MYC-driven cancers.

Maisano D, Wang T, Kulp SB et al. · Blood · (2026) · View on PubMed ↗

Phase 3 Trial of Weekly Oral Islatravir-Lenacapavir for HIV-1 Treatment.

This phase 3, double-blind, randomized, active-controlled noninferiority trial evaluated switching from once-daily bictegravir/emtricitabine/tenofovir alafenamide to once-weekly oral islatravir–lenacapavir (ISL/LEN) in adults with HIV-1 virologic suppression for at least 6 months across 12 countries. The key finding was the efficacy and safety of the weekly regimen compared with continued standard therapy, using noninferiority testing for virologic outcomes. Clinically, it addresses adherence challenges by testing a long-acting oral combination that could reduce dosing frequency while maintaining viral suppression.

Rockstroh JK, Ramgopal MN, Curran Fàbregas A et al. · The New England journal of medicine · (2026) · View on PubMed ↗

COMMIT: A Randomized Study of mFOLFOX6/Bevacizumab/Atezolizumab or Atezolizumab Alone as First-Line Treatment of Deficient DNA Mismatch Repair Metastatic Colorectal Cancer.

This randomized phase III open-label trial (NRG-GI004/SWOG-S1610, COMMIT) studied first-line treatment strategies for deficient DNA mismatch repair (dMMR)/microsatellite instability-high (MSI-H) metastatic colorectal cancer (mCRC) by comparing mFOLFOX6 plus bevacizumab plus atezolizumab versus atezolizumab alone. The key finding was the trial’s evaluation of whether adding chemotherapy and VEGF inhibition to PD-L1 blockade improves outcomes in a population where single-agent PD-1 therapy often leads to progression within 12 months. Scientifically and clinically, it tests a chemo-VEGF–immunotherapy synergy approach to improve survival and response rates in dMMR/MSI-H mCRC.

Rocha Lima CMSP, Yothers G, George TJ et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Exploring the Role of Surgery After Systemic Therapy in Locally Advanced Biliary Tract Cancer: Outcomes From a Large Retrospective Multinational Real-World Cohort Treated With Cisplatin, Gemcitabine, and Durvalumab.

This retrospective multinational real-world cohort study evaluated outcomes of surgery after response to first-line systemic therapy in locally advanced biliary tract cancer (BTC) treated with cisplatin, gemcitabine, and durvalumab (CGD). Across 55 centers in 12 countries, the analysis assessed overall survival, progression-free survival, and disease-free survival among resected patients, and modeled the prognostic impact of surgery using multivariable logistic regression to predict surgical candidacy. The findings provide evidence on whether and for whom surgery may add benefit after CGD response in initially unresectable locally advanced BTC.

Rimini M, Lamarca A, Ikeda M et al. · International journal of cancer · (2026) · View on PubMed ↗

Matching-adjusted indirect comparison of enzalutamide versus apalutamide with androgen-deprivation therapy in patients with metastatic hormone-sensitive prostate cancer.

This matching-adjusted indirect comparison (MAIC) compared enzalutamide plus androgen-deprivation therapy (ADT) versus apalutamide plus ADT in patients with metastatic hormone-sensitive prostate cancer (mHSPC) with ≥1 bone metastasis, using individual patient data from ARCHES (enzalutamide+ADT; n=971) matched to TITAN (apalutamide+ADT; n=1052). The analysis estimated comparative overall survival (OS), radiographic progression-free survival (rPFS), and time to PSA progression (TTPP) after adjusting for baseline differences, using Cox regression with placebo+ADT as the common comparator. This provides decision-relevant comparative effectiveness evidence for choosing between androgen receptor pathway inhibitors in mHSPC when head-to-head data are unavailable.

Azad AA, Pandya BJ, Bhadauria HS et al. · Future oncology (London, England) · (2026) · View on PubMed ↗

Efficacy and Safety of Two-Weekly Enfortumab Vedotin in Combination With Pembrolizumab for Advanced Urothelial Carcinoma.

This retrospective real-world study evaluated two-weekly enfortumab vedotin (EV) at 1.25 mg/kg combined with pembrolizumab (PEM) in treatment-naïve patients with metastatic advanced urothelial carcinoma (UC). It found a high objective response rate (75%) with a safety profile consistent with EV-related toxicities that often drive treatment modifications, though the abstract truncation limits full quantitative AE reporting. The significance is that a more frequent (two-weekly) EV schedule may be a feasible first-line option in routine practice while balancing efficacy and tolerability.

Nakagawa R, Izumi K, Toshima K et al. · Asia-Pacific journal of clinical oncology · (2026) · View on PubMed ↗

Real-world efficacy and safety of CDK4/6 inhibitors plus endocrine therapy in HR+/HER2 - metastatic breast cancer: a single-institution experience.

This retrospective single-institution study evaluated real-world efficacy and safety of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors—palbociclib, ribociclib, or abemaciclib—plus endocrine therapy in patients with HR+/HER2− metastatic breast cancer treated at Electricity Hospital, Cairo, Egypt. The key finding was that CDK4/6 inhibitor plus endocrine therapy showed clinically meaningful effectiveness and an acceptable safety profile in routine practice, consistent with prior trial evidence despite real-world variability. The results support the use of CDK4/6 inhibitors in broader clinical settings and help inform expectations for outcomes and tolerability outside controlled trials.

Hussein NE, Gad AM, AbdAllah A et al. · Journal of the Egyptian National Cancer Institute · (2026) · View on PubMed ↗

Transcription factor EN1 governs a lipogenic USP18-ACLY axis to drive bladder cancer malignancy.

The study examined how the transcription factor Engrailed-1 (EN1) drives metabolic reprogramming in bladder cancer (BLCA) and tested a drug candidate targeting this axis. It found that EN1 upregulates the deubiquitinase USP18, which prevents proteasomal degradation of ATP-citrate lyase (ACLY) to stabilize ACLY and enhance de novo lipogenesis, and that the FDA-approved drug udenafil suppresses the USP18/ACLY axis to inhibit BLCA malignancy. These results position the EN1–USP18–ACLY lipogenic pathway as a mechanistic vulnerability and suggest udenafil as a repurposing candidate for BLCA.

Zhan Y, Zhu C, Li Y et al. · Oncogene · (2026) · View on PubMed ↗

Genomics, sequencing, and molecular diagnostics/biomarkers

Cross-Ancestry Proteogenomic Analyses Identified New Therapeutic Insights for Ischemic Heart Disease.

This study used cis-acting protein quantitative trait loci (cis-pQTLs) for plasma proteins measured by Olink/SomaScan in statin-free participants from the China Kadoorie Biobank (1,976 incident ischemic heart disease cases and 2,001 controls) and leveraged cross-ancestry data from East Asians and Europeans to identify therapeutic targets for ischemic heart disease. The key finding was that proteogenomic cross-ancestry analyses highlighted new druggable protein targets beyond statin therapy, supported by genetic evidence from cis-pQTLs. These results provide a precision medicine framework for prioritizing novel repurposable targets for ischemic heart disease using ancestry-diverse proteogenomics.

Mazidi M, Wright N, Pozarickij A et al. · Journal of the American College of Cardiology · (2026) · View on PubMed ↗

Predictive immunohistochemistry in non-small cell lung cancer - Biomarkers, companion diagnostics, and molecular testing: A narrative review.

This narrative review studied the clinical utility of predictive immunohistochemistry (IHC) biomarkers in non-small cell lung cancer (NSCLC), including how assays, scoring systems, and companion diagnostic algorithms are used for molecular testing confirmation. The key finding was that predictive IHC performance and the need for molecular confirmation vary by biomarker, with detailed discussion of validated approaches for targets such as PD-L1 and oncogenic drivers including ALK, ROS1, and c-Met. This is significant for optimizing precision oncology workflows by aligning IHC testing strategies with regulatory guidance and biomarker-specific evidence.

Vranić S, Rose I, Kuzmova N et al. · Biomolecules & biomedicine · (2026) · View on PubMed ↗

Time-dependent prognostic value of automated Ki67 assessment and its integration with molecular risk profiling in WHO grade 2 meningioma.

This study evaluated whether automated, artifact-adjusted Ki67 assessment (QuPath-based pipeline with HistoART) and its integration with molecular risk profiling (DNA methylation and copy number) improves prognostication in 98 WHO grade 2 meningiomas (WHO 2021). It found that Ki67’s prognostic value can be time-dependent and that combining automated Ki67 with an integrated molecular-morphologic risk score (Maas et al.) better captures heterogeneous clinical courses. Clinically, this supports more robust risk stratification for grade 2 meningioma patients by standardizing Ki67 measurement and adding molecular context.

Voßbeck L, Ehret F, Perez E et al. · Acta neuropathologica communications · (2026) · View on PubMed ↗

Transcriptional evidence of neuroendocrine cell plasticity beyond histological boundaries in lung neuroendocrine neoplasms: an in-silico analysis suggesting a progression model.

This in-silico transcriptomic analysis examined whether lung neuroendocrine neoplasms (205 pulmonary neuroendocrine tumors [NETs] and neuroendocrine carcinomas [NECs]) show neuroendocrine cell plasticity beyond histological boundaries. Using supervised clustering of a curated 20-gene neuroendocrine differentiation/oncogenic/chromatin/lineage signature, it identified two clusters (PNEN-A and PNEN-B) and showed that PNEN-B has reduced neuroendocrine features independent of histology, consistent with a progression model. Scientifically, this suggests a molecular continuum across NET/NEC categories that could inform future staging and targeted therapeutic development.

Pelosi G, Papotti M, Papa R et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗

Global economic burden of depression in 154 countries from 2025 to 2050.

This multi-ancestry genome-wide association study (GWAS) meta-analysis examined fibromyalgia genetic architecture in 2,563,755 individuals (54,629 cases and 2,509,126 controls) across 11 cohorts. It identified 26 fibromyalgia risk loci, with the strongest signal at a coding variant in HTT (the causal gene for Huntington’s disease), and implicated HTT regulators such as GPR52 plus neural genes including DCC, DRD2/NCAM1, MDGA2, and CELF4. The study is significant because it shows brain/neural-tissue heritability enrichment and provides actionable targets for mechanistic research and potential future risk stratification.

Cao Z, Luo Y, Jiao L et al. · Nature medicine · (2026) · View on PubMed ↗

The DNA damage response and cancer immunotherapy.

This case report assessed whether tofersen, an antisense oligonucleotide approved for ALS due to pathogenic SOD1 variants, can be used to target a variant of uncertain significance (VUS) in SOD1. In a patient with respiratory-onset ALS carrying a novel SOD1 c.234_236del p.(Glu79del) VUS, six months of tofersen reduced CSF SOD1 protein by 47% and lowered CSF and serum NfL by 55% and 50%, respectively, with slowed ALSFRS-R decline compared with the pre-treatment period. The clinical significance is that it provides preliminary evidence that VUS-directed tofersen therapy may produce target engagement and biomarker effects comparable to those seen with pathogenic SOD1 variants.

Hong S, Li GM · Nature reviews. Cancer · (2026) · View on PubMed ↗

Consensus recommendations for next-generation sequencing-based genetic testing in Rare Neurological diseases.

This consensus guideline article developed recommendations for next-generation sequencing (NGS)-based genetic testing in rare neurological diseases (RND) using an external quality assessment (EQA) program. It identified 28 report-quality and process topics grouped into clinical information, interpretation, methodology, and reporting, using an adapted Delphi approach with 31 experts informed by EQA findings showing variability and limitations in genetic testing reports. The significance is that it aims to harmonize and improve the quality, completeness, and interpretability of NGS diagnostic reports for RND patients.

Maver A, Lohmann K, Urbanczyk LM et al. · European journal of human genetics : EJHG · (2026) · View on PubMed ↗

The genetics of fibromyalgia and its relationships to psychiatric and medical traits.

This genetic association study examined the genetics of fibromyalgia and its relationships to psychiatric and medical traits by conducting GWAS in European, African, and Latin American ancestry groups (85,139 cases; 1,642,433 controls) and applying multi-trait analysis of GWAS (MTAG) using pain GWAS to increase power. It identified multiple fibromyalgia-associated loci across ancestries (including 10 loci in European ancestry, one in African ancestry, and additional cross-ancestry loci) and used multi-trait methods to quantify genetic overlap with psychological and physiological phenotypes. These results clarify fibromyalgia’s polygenic architecture and shared genetic contributions with related traits, informing future mechanistic studies and risk stratification.

Bright U, Beck S, Levey DF et al. · Nature communications · (2026) · View on PubMed ↗

Cell therapy, CAR-T, and immune effector toxicity

Robust CD4+ CAR T cell expansion is associated with non-ICANS neurotoxicities after ciltacabtagene autoleucel in patients with multiple myeloma.

This cohort study evaluated predictors of non-immune effector cell-associated neurotoxicity syndrome (NINTs) in 109 patients with relapsed/refractory multiple myeloma treated with the CD19 CAR T cell therapy ciltacabtagene autoleucel (cilta-cel). High-peak absolute lymphocyte count was identified as a strong predictor of NINTs and correlated with peripheral-blood CAR T cell quantification by flow cytometry. These findings support using simple lymphocyte metrics to stratify neurotoxicity risk and guide mitigation strategies for cilta-cel recipients.

Jurgens EM, Mitra S, Herrera K et al. · Science translational medicine · (2026) · View on PubMed ↗

Virology, infectious disease, and host-pathogen interactions

Gasdermin E couples viral pyroptosis to lethal hepatic lipid accumulation.

This mechanistic virology study investigated how gasdermin E (GSDME) links viral pyroptosis to lethal hepatic lipid accumulation during infection with tick-borne orthonairoviruses, including wetland virus (WELV), in patient samples and experimental models. The key finding was that WELV triggers GSDME-dependent hepatocyte pyroptosis via mitochondrial and Fas-mediated apoptotic pathways, with viral RNA activating RIG-I/CASP3-mediated GSDME cleavage and viral nucleoprotein undergoing CASP3-dependent processing that forms a negative feedback loop. Scientifically, it identifies a GSDME–CASP3 axis that couples inflammation to fatty acid synthase (FASN)-associated lipid dysregulation, suggesting a targeted pathway for preventing fatal liver dysfunction.

Wang C, Zheng X, Zhang Y et al. · Cell · (2026) · View on PubMed ↗

A fungal effector inhibits plant MAPK signaling by acting as a decoy substrate of MKK5.

This study investigated how the secreted fungal effector VdHCE1 from Verticillium dahliae suppresses plant MAPK signaling during infection. VdHCE1 binds the MAPK kinase MKK5, is phosphorylated at threonine 166 in planta, and competes with MPK3/MPK6 as an MKK5 substrate to attenuate downstream MAPK activation. The work identifies a decoy-substrate mechanism that could be targeted to improve control of fungal phytopathogens.

Liu XQ, Liu XP, Jin L et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Integrated Single-Cell and TCR Profiling Reveals Protection-Associated CD8+ T Cell Subsets Linked to Viral Control in PRRSV.

This study used integrated single-cell RNA sequencing and T cell receptor (TCR) profiling in a porcine reproductive and respiratory syndrome virus (PRRSV) vaccination-challenge model to identify immune correlates of protection. Protected animals vaccinated with a modified live vaccine (MLV) showed enrichment of specific CD8+ T cell subsets with clonal expansion, strong cytotoxic transcriptional programs, and enhanced functional activity linked to rapid viral control. These data define protection-associated CD8+ T cell signatures that can guide improved PRRSV vaccine design and evaluation.

Kong C, Chen S, Li M et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Human lungs maintain tissue-resident memory T cells against a broad spectrum of pathogens.

The study investigated whether the mouse paradigm of rapid attrition of lung tissue-resident memory T (TRM) cells holds in humans by profiling T cells from human lungs across 40 individuals. Using a T-cell-receptor (TCR)–guided approach that combined single-cell transcriptomics with paired TCR repertoire profiling, the authors mapped pathogen specificity of >87,000 lung T cells and found that many individuals harbor TRM cells specific to multiple pathogens. This demonstrates that human lungs maintain TRM immunity broadly, informing vaccine and immunotherapy strategies aimed at durable mucosal protection.

Fajardo-Rosas V, Ehtram A, Marchand-Casas I et al. · Nature immunology · (2026) · View on PubMed ↗

Camel Prion Disease, Tataouine, Tunisia, 2019-2021.

This report investigated camel prion disease in dromedary camels in Tataouine, Tunisia, during 2019–2021, describing clinical and pathological findings in affected animals. Six cases were identified, with neurologic signs and disease-associated prion protein accumulation in brain and lymphoid tissues, confirming widespread occurrence in North Africa. The study underscores the need for active surveillance and epidemiologic investigation to clarify transmission routes and public health implications of camel prion disease.

Amara A, Di Bari MA, Elmehatli K et al. · Emerging infectious diseases · (2026) · View on PubMed ↗

Plant biology, microbiomes, and phytopathogen control

In situ structures of plant photosystem supercomplexes.

This study used in situ cryo-electron microscopy to determine native photosystem supercomplex structures in rice (Oryza sativa) chloroplasts. The authors resolved a C2S2M2L4-type PSII–LHCII supercomplex containing four LHCII antenna trimers that were not retained in purified preparations. These native structural insights are important for understanding excitation energy transfer in real chloroplast membrane environments and for improving models of photosynthetic efficiency.

Li J, Elias E, Zhang K et al. · Nature · (2026) · View on PubMed ↗

Intestinal stem cells count self-renewal divisions to switch multipotency.

This study investigated how Drosophila intestinal stem cells (ISCs) maintain a constant enteroendocrine cell (EEC) to enterocyte (EC) ratio during repeated divisions. It found that ISCs intrinsically count self-renewal divisions via an epigenetic mechanism to switch multipotency, producing enteroendocrine mother cells (EMCs) after a defined number of divisions. The work is significant because it provides a mechanistic basis for how stem cells use division-counting to regulate tissue composition under rapid turnover.

Tong D, Li A, Jiang Q et al. · Nature · (2026) · View on PubMed ↗

ATGL-mediated lipid droplet lipolysis promotes collective migration in Drosophila.

This in vivo Drosophila study investigated how ATGL-mediated lipid droplet (LD) lipolysis regulates collective border cell migration, using ATGL loss-of-function, knockdown, and overexpression in the Drosophila border cell model. ATGL loss increased LD volume and disrupted mitochondrial function, while ATGL depletion or overexpression delayed migration and impaired delamination, indicating that properly tuned LD lipolysis is required for efficient collective migration. The results link conserved LD lipase biology to invasive collective cell behavior, informing mechanistic understanding relevant to cancer metastasis.

Wipf IJ, Lowden EJ, Giedt MS et al. · Development (Cambridge, England) · (2026) · View on PubMed ↗

TIE1 acts as a maternal brake on fertilization-independent endosperm development by associating with PRC2 to enforce imprinting.

This plant genetics study investigated how the maternally expressed transcriptional repressor TIE1 controls fertilization-independent endosperm development in Arabidopsis by enforcing imprinting through interaction with PRC2 (polycomb repressive complex 2). It showed that disrupting four TIE genes (tie1 tie2 tie3 tie4; tieQ mutants) triggers autonomous endosperm development, and that TIE1 exhibits maternal genomic imprinting similar to MEDEA (MEA), a core FIS-POLYCOMB REPRESSIVE COMPLEX 2 component. The work clarifies a maternal “brake” mechanism on apomixis-like seed development, informing strategies to engineer clonal seed production for crop hybrid vigor.

Zhang Z, Wang X, Yuan R et al. · Nature plants · (2026) · View on PubMed ↗

Machine learning reveals biocontrol agents shaping disease outcome in natural Arabidopsis populations.

This ecological genomics study used six generations of leaf-microbiome data from natural Arabidopsis populations infected with the oomycete Albugo laibachii to determine how biocontrol agents shape disease outcomes. It showed that infection, site, and host genotype drive microbial diversity and that infected plants form modular networks with increased inter-kingdom antagonism, while machine-learning models identified microbiota features that discriminate infected versus uninfected plants and microbes enriched in diseased versus healthy plants. The findings support a data-driven route to rational biocontrol selection by linking specific microbial candidates to disease suppression in natural host populations.

Mahmoudi M, Hu Y, Almario J et al. · Nature communications · (2026) · View on PubMed ↗

Bioengineering methods and omics technologies

AAV2 bypasses direct endosomal escape by using AAVR to access the trans-Golgi network en route to the nucleus.

This mechanistic study investigated adeno-associated virus type 2 (AAV2) intracellular trafficking in vitro, focusing on the role of the AAV cell entry receptor AAVR in bypassing direct endosomal escape and routing to the trans-Golgi network en route to the nucleus. The key finding was that AAVR acts as a bona fide retromer cargo: its cytosolic tail engages the retromer–SNX3 complex to drive membrane tubulation, and in AAVR-knockout HuH-7 cells AAV2 internalization/trafficking is impaired. These findings refine AAV gene-delivery models by identifying a retromer-dependent retrograde pathway as a key trafficking route.

Cabanes-Creus M, Liao SHY, Pardo-Piñón M et al. · Journal of virology · (2026) · View on PubMed ↗

An In Vitro Quantitative Systems Pharmacology Platform for Characterizing CD3-Bispecific Antibody-Mediated T-Cell Activation and Tumor Cell Cytotoxicity.

The study developed an in vitro quantitative systems pharmacology (QSP) platform to mechanistically characterize CD3-bispecific antibody (CD3-BsAb)–mediated T-cell activation and tumor cell cytotoxicity across heterogeneous laboratory assay conditions. The model integrates single-cell trimer-formation dynamics and other key steps to enable quantitative, cross-protocol comparisons of CD3-BsAb potency and activity. This provides a standardized, mechanistic framework to accelerate CD3-BsAb candidate selection and improve translational predictability from in vitro assays.

Yuan X, Thalhauser C, Afzal N et al. · The AAPS journal · (2026) · View on PubMed ↗

AI proteomics: from protein identification to virtual cells.

This Perspective discusses how artificial intelligence (AI) is being applied to mass spectrometry (MS)-based proteomics, spanning protein identification/quantification, protein-protein interactions and complexes, spatial and perturbation proteomics, and multi-omics integration. It highlights that AI-driven methods are increasingly enabling end-to-end workflows and “AI virtual cells” that model biological states from proteomic data. The work is significant because it frames an AI-friendly ecosystem for MS proteomics that could accelerate discovery and improve reproducibility across data producers and consumers.

Sun Y, A J, Liu Z et al. · Nature methods · (2026) · View on PubMed ↗

Sequencing-free spatial profiling of post-transcriptional regulation in fresh tissues using nanoneedle arrays.

This study developed a sequencing-free and amplification-free spatial profiling method for post-transcriptional regulation in fresh tissues using nanoneedle arrays. By extracting RNA molecules from individual cells while preserving spatial organization and using multiplexed fluorescence encoding with imaging-based decoding, it quantified mRNAs, microRNAs, and N6-methyladenosine (m6A)-modified RNAs across large tissue sections. The scientific significance is that it enables spatial epitranscriptomics and post-transcriptional mapping without the cost and workflow complexity of sequencing, potentially improving access to fresh-tissue analyses.

Ji X, Fang P, Wan Y et al. · Nature biomedical engineering · (2026) · View on PubMed ↗

Tissue models, organoids, and spatial/3D mapping

A spatially organized immune-stromal program drives the fissure-to-fistula continuum in Crohn’s disease.

This study used spatial transcriptomics on intestinal surgical specimens from Crohn’s disease patients spanning inflamed tissue, fissures of increasing depth, and entero-enteric fistulas to define spatial immune–stromal interactions driving the fissure-to-fistula continuum. By integrating spatial data with single-cell references and ligand–receptor analyses, the authors identified organized immune–stromal programs associated with progression from fissure formation to fistulizing disease. The work provides mechanistic, tissue-level targets that could guide biomarker development and more precise interventions for fistulizing Crohn’s disease.

Massimino L, Nicolò S, Parigi TL et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.

This article provides integrative insights from spatial transcriptomics to understand sepsis-associated acute kidney injury (SA-AKI), emphasizing the need for spatial context beyond bulk, single-cell RNA-seq, and proteomics. It highlights how combining high-resolution spatial transcriptomics with single-cell RNA sequencing can resolve immune, vascular, and parenchymal heterogeneity and microenvironmental changes during SA-AKI. Scientifically, it supports more precise mechanistic mapping of SA-AKI and can guide development of targeted therapies informed by tissue architecture.

Uhlig M, Schumacher D, Marx G et al. · Nature reviews. Nephrology · (2026) · View on PubMed ↗

Core2Edge: a human glioblastoma organoid-brain slice model capturing infiltration and transcriptional heterogeneity from core to single-cell dispersion.

This Nature Protocols article describes Core2Edge, a fully human glioblastoma organoid–brain slice ex vivo model designed to capture tumor infiltration and transcriptional heterogeneity from the core to single-cell dispersion. The model is intended to reproduce the infiltration spectrum and malignant connectivity across distances in a human tissue context, addressing limitations of animal models and ethical concerns. Its significance is that it provides a scalable platform for studying invasion biology and testing therapies in a more human-relevant infiltration setting.

Melhem A, Pregler BEF, Rodriguez-Gatica JE et al. · Nature protocols · (2026) · View on PubMed ↗

Mechanobiology and mechanosensitive immune regulation

Mechanosensitive ion channels in immunity from biophysics to mechanomedicine.

This 2026 review synthesized evidence that mechanosensitive ion channels (MSICs)—including Piezo, TRPV4, K2P/TREK, TMEM63/OSCA, and ENaC—act as molecular transducers of mechanical cues in immune cells. It highlights that MSIC gating converts mechanical forces into Ca2+ and K+ fluxes that regulate transcriptional and effector immune programs, positioning MSICs as “mechanical immune checkpoints.” The review frames how mechanobiology can be leveraged for mechanomedicine approaches to modulate immune function in disease.

Zhang H, Jiang D, Mou Y et al. · Biophysical journal · (2026) · View on PubMed ↗

Hematology and clonal hematopoiesis malignancies

Blastic plasmacytoid dendritic cell neoplasm: ontogeny, immunophenotype, genetics and epigenetics, immune dysregulation, skin tropism and therapeutic implications.

This review article synthesizes evidence on blastic plasmacytoid dendritic cell neoplasm (BPDCN) ontogeny, immunophenotype, genetics, epigenetics, immune dysregulation, skin tropism, and therapeutic implications in the context of hematopoietic stem/progenitor biology. It concludes that BPDCN is a distinct hematologic malignancy that commonly originates from hematopoietic stem or progenitor cells with clonal hematopoiesis (CH)-associated mutations, clarified by advances in immunophenotyping, transcriptional profiling, and genomic analysis. These mechanistic insights support more precise diagnostic stratification and rational therapeutic targeting of the underlying clonal and epigenetic programs driving aggressive skin-tropic disease.

Xia C, Pradhan D, Wang W et al. · Leukemia · (2026) · View on PubMed ↗

Musculoskeletal biology, osteoarthritis, and bone remodeling

Osteocyte-specific gasdermin D deletion accelerates osteoarthritis via promoting subchondral inflammation and remodeling.

This experimental study tested whether osteocyte-derived gasdermin D (GSDMD) regulates subchondral bone homeostasis and contributes to osteoarthritis (OA) remodeling by using osteocyte-specific GSDMD deletion in clinical and experimental OA models and osteocyte co-culture systems. It found that osteocyte-specific GSDMD deletion accelerates OA by promoting subchondral inflammation and pathological remodeling, consistent with GSDMD expression in osteocytes in OA. The results extend GSDMD’s role beyond immune-cell pyroptosis to osteocyte-driven inflammatory remodeling, identifying osteocyte GSDMD as a potential therapeutic target to slow early OA progression.

Ogawa Y, Ebata T, Tokuhiro T et al. · Bone research · (2026) · View on PubMed ↗

Reproductive biology and 3D genome architecture

High-resolution chromatin mapping reveals that CTCF anchors meiotic loops to the chromosome axis.

This study mapped meiotic chromatin architecture in mouse germ cells by using high-resolution Hi-C and Micro-C across the transition from spermatogonia to spermatocytes. It found that meiotic chromatin reorganization—including a shift from mitotic-to-meiotic cohesins and loss of large-scale A/B compartments—occurs before the traditionally defined meiotic entry point (meiotic G1/S-phase), and that CTCF anchors distinct meiotic loops to the chromosome axis. These mechanistic insights refine models of how 3D genome organization is established during meiosis and how regulatory elements are positioned to control gene expression during gametogenesis.

Cheng G, Li X, Brick K et al. · Nature communications · (2026) · View on PubMed ↗

Aging, senescence, and mitochondrial quality control

Senotypes define the diverse landscape of senescent cells.

This work proposed and operationalized the concept of “senotypes” to classify senescent cells across cell types, senescence-inducing stresses, tissue contexts, and time. The authors provided a framework integrating cell identity/context, inducing mechanism, temporal stage, multimodal molecular/structural features, and physiological/pathological functions to organize senescence heterogeneity. This classification scheme is significant because it enables more precise experimental comparisons and may guide senolytic/senomorphic strategies by targeting specific senescent cell states rather than senescence broadly.

Schafer MJ, Basisty N, Hertzel AV et al. · Nature aging · (2026) · View on PubMed ↗

The glycolytic enzyme PGAM1 functions as a metabolic-autophagy checkpoint to coordinate growth and stress tolerance.

The study investigated the conserved glycolytic enzyme PGAM1 in yeast and mammalian systems to determine how it coordinates glycolysis with autophagy initiation. PGAM1 acted as a metabolic–autophagy checkpoint by functioning as a molecular scaffold that recruits the phosphatidylinositol 3-kinase complex I to the phagophore assembly site, licensing autophagosome biogenesis independently of its catalytic activity. This genetically essential, evolutionarily conserved mechanism links metabolic state to autophagy control and identifies PGAM1 as a potential lever for growth–stress tolerance regulation.

Zhang Y, Zhao P, Liang H et al. · Nature cell biology · (2026) · View on PubMed ↗

Proteomic organ-specific signatures, ageing traits, disease risks and genetic architecture in an East Asian population.

This prospective EBioMedicine study analyzed proteomic organ-specific signatures of aging in an East Asian population using plasma proteomics from the China Kadoorie Biobank (about 4000 individuals) measured by Olink and SomaScan. The key finding was that Light Gradient Boosting models trained on chronological age (ChronAge) produced organ-level protein age gaps (ProtAgeGap) that related to age-related traits, disease risks, and genetic architecture, leveraging organ-enriched plasma proteins from GTEx. Scientifically, it extends protein-based aging clocks to non-European populations and integrates multi-platform proteomics with genetic and disease associations.

Bennett DA, Wang B, Xiao S et al. · EBioMedicine · (2026) · View on PubMed ↗

Nuclear class 3 PI3K co-activates fasting-specific chromatin remodelling.

This study investigated how nuclear class 3 PI3K (PI3K-3) regulates fasting-induced transcriptional and chromatin remodeling. It found that nuclear PI3K-3 acts as a co-activator of epigenetic writers by overlapping with transcriptionally engaged RNA polymerase II phosphorylated at Ser5 and with the Setd1a/COMPASS complex that deposits the activating H3K4me3 mark, thereby promoting RNAPII transcription during fasting. The significance is that it links nutrient sensing to specific chromatin-writing machinery, identifying PI3K-3 as a direct chromatin co-activator in fasting responses.

Henneman NF, Kawamura G, Luo Y et al. · Nature cell biology · (2026) · View on PubMed ↗

Fractionated proteomics identifies a protein network mitigating resistance exercise-induced damage in human skeletal muscle.

This human proteomics study investigated molecular networks that mitigate resistance exercise-induced damage in skeletal muscle by applying fractionated proteomics to repeated muscle sampling during acute, repeated, interrupted resistance exercise. It found dynamic changes in the protein landscape associated with the sarcomeric cytoskeleton that correlate with phosphorylation signatures of adaptation and deadaptation signaling. The identified protein network provides mechanistic targets for improving recovery and reducing exercise-induced muscle injury.

Kuppusamy M, Jacko D, Gupta Y et al. · Nature communications · (2026) · View on PubMed ↗

Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.

This review article summarizes mitochondrial quality control mechanisms in health and disease, focusing on how mitochondrial proteostasis, dynamics, mitophagy, and related pathways contribute to metabolism, apoptosis, inflammation, proliferation, and redox balance. It highlights that mitochondrial dysfunction is implicated across many human diseases and frames mitochondrial quality control components as therapeutic targets. The synthesis supports translational efforts to develop interventions that preserve mitochondrial integrity to treat diverse mitochondrial-linked pathologies.

Creus A, Mohapatra S, Ortega L et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

Dermatology therapeutics (psoriasis/eczema/alopecia)

Antihistamines for atopic dermatitis (eczema): systematic review and network meta-analysis of randomised trials.

This systematic review and network meta-analysis synthesized randomized trials of add-on oral H1 antihistamines, H2 blockers, and mast cell stabilizers (nedocromil sodium and sodium cromoglycate) for atopic dermatitis in patients with eczema. The key finding was the comparative evidence base for benefits and harms across these oral add-on options, synthesized using network meta-analysis (with relative effects and safety signals derived from the included randomized comparisons). Clinically, the results aim to guide evidence-based selection of oral adjunct therapies for atopic dermatitis beyond topical treatment by clarifying which drug classes have the most favorable benefit–harm profiles.

Chu AWL, Wen A, Guyatt GH et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

The role of aryl hydrocarbon receptor agonists in the management of inflammatory skin diseases: An expert consensus panel.

This expert consensus panel evaluated the evidence for tapinarof, a nonsteroidal aryl hydrocarbon receptor (AhR) agonist, in managing inflammatory skin diseases such as psoriasis and atopic dermatitis. The panel concluded that AhR agonists like tapinarof provide effective, steroid-sparing options that can be used for longer durations and on sensitive skin sites, complementing guideline-based topical corticosteroid use. These recommendations support safer long-term treatment strategies for chronic inflammatory dermatoses by clarifying where tapinarof fits relative to topical corticosteroids and other nonsteroidal therapies.

DeBusk L, Bartley B, Armstrong AW et al. · Dermatology online journal · (2026) · View on PubMed ↗

The efficacy and safety of interleukin-17 and interleukin-23 inhibitors in psoriatic arthritis across multiple disease domains.

This study systematically reviewed randomized trials, long-term extension data, mechanistic studies, and meta-analyses comparing IL-17 and IL-23 pathway inhibitors in psoriatic arthritis across clinical domains (peripheral joints, entheses, skin, and nails) in patients with heterogeneous disease and prior biologic failure. The review found clinically meaningful differences in efficacy between IL-17 and IL-23 inhibitors depending on the disease domain, with some agents showing stronger responses in specific manifestations. These findings help clinicians select biologic therapy more precisely for multisystem PsA and for patients with inadequate response to prior biologics.

Zakria D, Shah M, Rosenberg A et al. · Dermatology online journal · (2026) · View on PubMed ↗

Efficacy and Safety of Oral Janus Kinase Inhibitors in Adults and Adolescents with Alopecia Areata: A Systematic Review and Meta-Analysis of Randomised Controlled Trials.

This systematic review and meta-analysis of randomized controlled trials assessed oral Janus kinase (JAK) inhibitors versus placebo for moderate-to-severe alopecia areata in adults and adolescents. It concludes that oral JAK inhibitors improve clinical outcomes compared with placebo while also increasing the risk of adverse events typical of systemic JAK blockade. The significance is that it consolidates comparative efficacy and safety evidence to guide systemic treatment decisions for patients with more extensive alopecia areata.

Morriss S, Foo CH, Lin E et al. · American journal of clinical dermatology · (2026) · View on PubMed ↗

Gastroenterology (Crohn’s/UC/cirrhosis) and GI outcomes

Comparison of Factors Associated With 30-Day and 90-Day Readmission Among a Global Cohort of Patients Hospitalised With Cirrhosis.

This global cohort study examined factors associated with 30-day versus 90-day readmission outcomes in prospectively enrolled, non-electively hospitalized adults with cirrhosis across 125 centers in 37 countries (n=4,208). The key finding was that predictors of readmission and related outcomes (including liver transplantation and mortality) differ between the 30-day and 90-day post-discharge windows. This helps clinicians stratify risk and tailor post-discharge management timing to reduce avoidable readmissions in cirrhosis.

Idilman R, Haktaniyan B, Choudhury A et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗

Impact of 5-aminosalicylic acid intolerance on progression to difficult-to-treat ulcerative colitis: a retrospective cohort study.

The retrospective cohort study of 919 ulcerative colitis (UC) patients evaluated whether intolerance to 5-aminosalicylic acid (5-ASA) predicts progression to difficult-to-treat (D2T) UC and whether specific intolerance phenotypes and post-intolerance treatment status modify risk. Using cumulative incidence methods with competing risks (death and colectomy) plus multivariable adjustment and landmark analyses, the authors found that 5-ASA intolerance is associated with higher risk of progression to D2T disease. This supports early identification of 5-ASA intolerance phenotypes and informs treatment planning to prevent escalation to difficult-to-treat UC.

Ohno M, Nishida A, Yoshida S et al. · Journal of gastroenterology · (2026) · View on PubMed ↗

Oncology surgery, radiotherapy/locoregional strategies, and surveillance

Dynamic Circulating Tumor DNA Methylation Monitoring Guiding Postoperative Surveillance in Nonmetastatic Colorectal Cancer: A Prospective, Randomized, Phase III FIND Trial.

This prospective, multicenter randomized phase III FIND trial tested whether dynamic circulating tumor DNA (ctDNA) methylation monitoring improves postoperative surveillance in nonmetastatic colorectal cancer after curative resection. The key finding was that a ctDNA-guided strategy (with positive ctDNA triggering immediate CT imaging and negative results leading to continued bimonthly CT plus quarterly ctDNA testing) was evaluated against standard CT-based monitoring to increase the rate of curative-intent therapy for recurrence. Clinically, it assesses whether ctDNA methylation can enable earlier, more actionable detection of recurrence and improve treatment intent at relapse.

Mo S, Zhou C, Ma M et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Definition of Conversion Therapy and Neoadjuvant Therapy for Hepatocellular Carcinoma: A Consensus Guideline from the Japan Liver Cancer Association.

This consensus guideline from the Japan Liver Cancer Association studied how to define “conversion therapy” versus “neoadjuvant therapy” in patients with advanced hepatocellular carcinoma (HCC) in the context of modern systemic regimens such as lenvatinib, atezolizumab–bevacizumab, durvalumab–tremelimumab, and nivolumab–ipilimumab. The key finding was the establishment of a standardized, consensus-based definition to clarify when systemic therapy combined with locoregional modalities should be classified as conversion therapy. This improves comparability of clinical studies and supports more consistent treatment selection and reporting in advanced HCC.

Ichida A, Tateishi R, Hatano E et al. · Liver cancer · (2026) · View on PubMed ↗

Generated automatically on July 30, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.

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PubMed Trending Research Digest — July 30, 2026

PubMed Trending Research Digest — July 30, 2026

Overview

Diabetes, metabolic stress, and diabetic complications

Mitochondrial metabolism and epigenetic crosstalk drive SASP.

Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.

Methylmalonate Overload Despite Glycemic Control Drives Diabetic Heart Damage.

Joint effects of social determinants of health on NAFLD mortality: the mediating role of phenotypic age acceleration.

The accumulation of methylglyoxal and acrolein impairs arginine homeostasis causing hyperglycemia and renal abnormalities in male zebrafish.

Cardiovascular epidemiology and risk prediction

Antithrombotic treatment for migraine in patients with patent foramen ovale: multicentre, randomised, active controlled, open label trial.

Associations of accelerometer-derived daily step counts with future health risks: A phenome-wide association study among over 60,000 UK adults.

Anesthetic-Electrophysiologic Interactions: How Sedatives Shape Cardiac Conduction and Arrhythmia Risk.

Baseline versus cumulative cholesterol, high-density lipoprotein, and glucose index and stroke risk in individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: evidence from the CHARLS study.

Effect of empagliflozin on copeptin levels in patients with recent acute coronary syndrome and newly detected dysglycaemia: a post-hoc analysis of the SOCOGAMI randomized controlled trial.

Can baxdrostat redefine blood pressure control in resistant and uncontrolled hypertension? a systematic review, meta-analysis, and trial sequential analysis.

Racial and ethnic disparities in the cause of death for clear cell renal cell carcinoma.

Atherosclerosis and immune inflammation in cardiovascular disease

Soluble TREM2 Drives Atherosclerosis via HSP90β-Dependent Myeloid Inflammation.

Lipid biology and LDL-C burden

Effect of Acoramidis on Heart Failure-Related Health Status: A Secondary Analysis of the ATTRibute-CM Randomized Clinical Trial.

Global Burden of Elevated LDL-C: Findings From the Global Burden of Disease Study 2023.

Kidney disease, renal injury, and cardiorenal/reno-cardiac syndromes

Early Prediction of External Ventricular Drain Weaning Trial Outcome in Patients with SAH Based on ICP Pulse Morphological Similarity: A Single-Center Retrospective Cohort Analysis.

Acute cardio-renal and Reno-Cardiac syndromes in critical care.

Intracranial pressure physiology, monitoring and individualized management in the acute brain injured patient.

Identification of pulmonary hypertension with pulmonary vascular surface volume ratio by non-contrast CT.

Neurodegeneration and neuroinflammation (AD/PD/ALS/MS)

Transaldolase 1 contributes to pentose phosphate pathway disruption and synaptic dysfunction in Alzheimer’s disease.

Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer’s disease.

Disease Course After Anti-CD20 Discontinuation in Secondary Progressive Multiple Sclerosis-A Multicenter Long-Term Longitudinal Study.

Neuroinflammation in Alzheimer’s and Parkinson’s diseases: pathogenic mechanisms and therapeutic strategies.

Parkinson’s disease biomarkers and DBS-informed psychiatry

Subthalamic spatio-spectral-connectivity of psychiatric symptoms in Parkinson’s disease.

Greater Motor and Nonmotor Burden at Diagnosis Is Associated With Amyloid Copathology in Parkinson’s Disease.

Epilepsy and cGAS–STING innate immune signaling

cGAS-mediated type I IFN signaling contributes to disease progression in drug-refractory epilepsy.

Psychiatric disorders, suicidality, and trauma-related trajectories

Prior Sexual Violence, PTSD Symptoms, and Recovery Trajectories After New Trauma.

Oral Semaglutide for Alcohol Use Disorder: A Randomized Clinical Trial.

Mendelian Randomization Analysis of the IL-1 Cytokine Family Proteins Identifies IL1RL1 as a Potential Causal Contributor to Traumatic Brain Injury Prognosis.

Suicide in neurodegenerative diseases: a systematic review.

Convergent neuroimmune signaling underlying rapid antidepressant response to ketamine and psychedelics.

Genetically informed dissection of multimodal brain aging and ten major psychiatric disorders.

Pain mechanisms and chronic pain syndromes

Phase 2b Trial of a NaV1.8 Inhibitor for Acute Pain.

Common Mechanisms in Migraine, Migraine-Related Neck Pain, and Low Back Pain: Implications for Treatment.

Sleep disorders and circadian biology

Current and Emerging Therapies for Pediatric Sleep Disorders: A Narrative Review.

Evening Light-Emitting Diode Screen Exposure, Melanopsin-Mediated Circadian Disruption, and Optical Filtration for Sleep Hygiene: A Narrative Review in the Indian Context.

Cancer immunotherapy mechanisms and biomarkers

Functional Engineered Exosomes Loaded with Nanoenzymes Targeting the Proteasome and Inflammation for the Treatment of Rheumatoid Arthritis.

Binding of death receptor 3 (DR3) to intracellular TRADD and TRAF2 is independent of its natural ligand, TL1A.

Tailored FcγR blockade enhances immune checkpoint therapy and overcomes resistance.

A genome-wide CRISPR screen in human prostate cancer cells reveals drivers of macrophage-mediated cell killing and positions AR as a tumor-intrinsic immunomodulator.

The genetic architecture of fibromyalgia across 2.5 million individuals.

Cancer therapeutics and comparative effectiveness

A first-in-class RNA degrader reduces c-MYC expression and myeloma cell survival in preclinical models.

Phase 3 Trial of Weekly Oral Islatravir-Lenacapavir for HIV-1 Treatment.

COMMIT: A Randomized Study of mFOLFOX6/Bevacizumab/Atezolizumab or Atezolizumab Alone as First-Line Treatment of Deficient DNA Mismatch Repair Metastatic Colorectal Cancer.

Exploring the Role of Surgery After Systemic Therapy in Locally Advanced Biliary Tract Cancer: Outcomes From a Large Retrospective Multinational Real-World Cohort Treated With Cisplatin, Gemcitabine, and Durvalumab.

Matching-adjusted indirect comparison of enzalutamide versus apalutamide with androgen-deprivation therapy in patients with metastatic hormone-sensitive prostate cancer.

Efficacy and Safety of Two-Weekly Enfortumab Vedotin in Combination With Pembrolizumab for Advanced Urothelial Carcinoma.

Real-world efficacy and safety of CDK4/6 inhibitors plus endocrine therapy in HR+/HER2 - metastatic breast cancer: a single-institution experience.

Transcription factor EN1 governs a lipogenic USP18-ACLY axis to drive bladder cancer malignancy.

Genomics, sequencing, and molecular diagnostics/biomarkers

Cross-Ancestry Proteogenomic Analyses Identified New Therapeutic Insights for Ischemic Heart Disease.

Predictive immunohistochemistry in non-small cell lung cancer - Biomarkers, companion diagnostics, and molecular testing: A narrative review.

Time-dependent prognostic value of automated Ki67 assessment and its integration with molecular risk profiling in WHO grade 2 meningioma.

Transcriptional evidence of neuroendocrine cell plasticity beyond histological boundaries in lung neuroendocrine neoplasms: an in-silico analysis suggesting a progression model.

Global economic burden of depression in 154 countries from 2025 to 2050.

The DNA damage response and cancer immunotherapy.

Consensus recommendations for next-generation sequencing-based genetic testing in Rare Neurological diseases.

The genetics of fibromyalgia and its relationships to psychiatric and medical traits.

Cell therapy, CAR-T, and immune effector toxicity

Robust CD4+ CAR T cell expansion is associated with non-ICANS neurotoxicities after ciltacabtagene autoleucel in patients with multiple myeloma.

Virology, infectious disease, and host-pathogen interactions

Gasdermin E couples viral pyroptosis to lethal hepatic lipid accumulation.

A fungal effector inhibits plant MAPK signaling by acting as a decoy substrate of MKK5.

Integrated Single-Cell and TCR Profiling Reveals Protection-Associated CD8+ T Cell Subsets Linked to Viral Control in PRRSV.