PubMed Trending Research Digest — May 23, 2026

Automated digest · 97 articles · 15 research areas · May 23, 2026

Overview

This week’s digest is dominated by two cross-cutting trends: (1) precision targeting—using biomarkers, engineered biologics, and mechanism-based stratification—and (2) deeper mechanistic dissection of disease processes to identify tractable intervention points. In oncology and immunotherapy, multiple studies emphasize improving durability and specificity: bispecific and dual-target CAR T strategies for multiple myeloma and B-ALL, ADC–checkpoint combinations in TNBC, and mechanistic work on resistance (e.g., NECTIN4-ADC uptake failure; KRAS inhibitor resistance via genetic plus transcriptional state switching; ALDH2-marked resistant tumor-associated macrophages). Parallel clinical efforts standardize care for high-need subgroups (severe lung cancer consensus; EBUS/EUS staging recommendations; bladder cancer adjuvant radiotherapy trial design), while patient-centered outcomes (time toxicity for bispecific antibodies) highlight the growing focus on real-world burden.

On the biology side, several papers converge on “cell-state control” and intracellular logistics: lysosome sorting (Arl8b–Rab11a–TBC1D9B), axonal autophagy and α-synuclein clearance (PPM1H/RAB signaling), tRNAome remodeling as a functional switch for antiviral vs proviral translation, and NO-driven alternative splicing via PTBP1 conformational control. Neurodegeneration and neuroinflammation remain prominent, with mechanistic α-synuclein/PD work, improved DSAD modeling, and MS lesion profiling that identifies a foamy GPNMB+ microglia/macrophage program linked to lesion expansion. In parallel, metabolism and immune–metabolic interfaces continue to expand: GLP-1/tirzepatide evidence syntheses and pharmacovigilance signals, MASLD/MASH burden and mechanistic lipotoxicity pathways, and exercise biology framed as an immunotherapeutic lever.

Finally, the digest includes notable translational and public-health threads: imaging innovations targeting GPR84 for selective neuroinflammation monitoring, large-scale epidemiology and genetics (e.g., autoimmune disease–pregnancy risk; PD GWAS refinement in East Asians; clonal hematopoiesis risk stratification), and infectious disease preparedness (Ebola outbreak response acceleration; HBV entry receptor expansion; antiviral defense mechanisms). Together, these studies reinforce a broader theme: combining high-resolution measurement (omics, imaging, MRD assays) with mechanistic insight is increasingly central to both risk prediction and therapy development.

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Neurodegeneration & Dementia (including Parkinson disease, α-synuclein, LATE, DSAD)

Age-related behavioral and molecular landmarks in new mouse models for studying Alzheimer’s disease in Down syndrome.

This study developed and characterized two novel Down syndrome–associated Alzheimer’s disease (DSAD) mouse models with partial humanization of amyloid-β (Aβ) to address species-specific Aβ differences. The models showed age-related behavioral changes and molecular AD landmarks including cognitive deficits, tau hyperphosphorylation, and endolysosomal dysfunction. Scientifically, the work provides improved DSAD tools to study how APP gene triplication and additional Hsa21 factors drive early AD pathology and related phenotypes.

Baniowska MR, Mumford P, Prestia F et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

GRN rs5848 variant associates with TDP-43 pathology and cancer in opposite directions.

This study examined whether the GRN single-nucleotide variant rs5848 (T allele) associated with limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and hippocampal sclerosis of aging (HS-Aging) also related to cancer risk in the same cohort. The rs5848 T allele was linked to increased LATE-NC/HS-Aging pathology but showed an inverse (opposite-direction) association with cancer, consistent with lower progranulin (PGRN) expression. These findings suggest that GRN/PGRN biology may help explain the epidemiologic inverse relationship between dementia pathology and cancer risk.

Aung KZ, Nelson PT, Ning X et al. · Journal of neuropathology and experimental neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Knockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal autophagy and exacerbates alpha-synuclein aggregation.

This mechanistic study investigated how knocking out the LRRK2-counteracting RAB phosphatase PPM1H affects neuronal autophagy and alpha-synuclein (aSyn) pathology relevant to Parkinson disease. PPM1H knockout caused a gene-dose-dependent disruption of axonal autophagosome transport, impairing degradation of axonal aSyn and exacerbating its aggregation. These findings identify PPM1H as a regulator of axonal autophagy and suggest that restoring PPM1H/RAB signaling balance could be a therapeutic strategy to mitigate aSyn accumulation in PD.

Fricke M, Mechel A, Evers L et al. · Cell reports · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

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Neuroinflammation & CNS Disorders (MS, neuroinflammation imaging, tinnitus, sleep/dementia links)

Micro- and nanoplastics in the central nervous system: Transport pathways, neurotoxicity, and implications for brain disorders.

This review evaluated how micro- and nanoplastics (MNPs) may enter and exit the central nervous system (CNS)—including blood-brain barrier crossing, nasal-to-brain routes, and glymphatic transport—and how these pathways relate to neurotoxicity and brain disorders. It concludes that small-sized MNPs are difficult to clear from the brain and may therefore accumulate, potentially contributing to neurotoxic effects linked to multiple brain disorders. The synthesis highlights CNS transport and persistence mechanisms as key targets for future experimental studies and risk assessment of MNP exposure.

Jing W, Zheng M, Yang X et al. · Ecotoxicology and environmental safety · (2026) · View on PubMed ↗

Does inflammatory bowel disease play a role in cognitive decline? A systematic review.

This systematic review assessed whether inflammatory bowel disease (IBD) is associated with cognitive decline by evaluating observational and preclinical studies in human populations and experimental models. It reports that evidence remains controversial, with proposed contributors including chronic inflammation, gut-brain axis dysfunction, and psychological comorbidities that may influence cognitive outcomes. Clinically, the review underscores the need to clarify mechanisms and stratify risk factors so cognitive impairment can be better prevented and managed in IBD patients.

Motisi Bertulli A, Bezzio C, Marsano S et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

Viral associations in multiple sclerosis: pathogenetic mechanisms and therapeutic implications.

This review summarized evidence for viral associations in multiple sclerosis (MS), focusing on pathogenetic mechanisms and therapeutic implications, with emphasis on viruses with strong evidence such as Epstein-Barr virus and other Herpesviridae members (e.g., human herpesvirus 6 and varicella-zoster virus). It concludes that dysregulated immune responses and chronic inflammation triggered or shaped by specific viral infections may contribute to MS development and progression. The synthesis supports continued investigation of viral mechanisms as potential targets for prevention and treatment strategies in MS.

Meshref M, Hussein AS, Allam SA et al. · Virology journal · (2026) · View on PubMed ↗ · Free PDF ↗

Foamy microglia link oxylipins to disease progression in multiple sclerosis.

This study investigated multiple sclerosis lesion biology by profiling human postmortem secondary progressive MS lesions using integrated lipidomics, transcriptomics, proteomics, chemical proteomics, and histology to define foamy GPNMB+ microglia/macrophage states linked to lesion expansion. It found that lesions containing foamy microglia/macrophages show disrupted lipid metabolism, lysosomal stress, and increased phagocytosis/antigen-presentation markers without classical pro-inflammatory signatures, and these foamy cells associate with expanding lesions. The results are significant because they identify a specific microglia/macrophage program (foamy GPNMB+ cells) and oxylipin-linked pathways that may be targeted to slow MS progression.

van der Vliet D, Di X, Shamorkina TM et al. · Nature neuroscience · (2026) · 7 citations · View on PubMed ↗ · Free PDF ↗

The exercise hormone irisin has neuroprotective effects in a mouse model of multiple sclerosis.

This study examined whether the exercise hormone irisin mediates neuroprotection in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis, using wild-type mice and mice lacking Fndc5/irisin (the irisin precursor). Voluntary free-wheel running protected against inflammation-induced neurodegeneration in EAE, but this protection was abrogated in Fndc5/irisin-deficient mice, and peripheral irisin delivery increased plasma irisin while reducing clinical symptoms and neuronal loss. These results support a causal, Fndc5/irisin-dependent pathway linking aerobic exercise to neuroprotection in MS models and suggest irisin as a potential therapeutic or biomarker target.

Rosenkranz SC, da Rocha JF, Moreira L et al. · Nature metabolism · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Tinnitus.

This Nature Reviews Disease Primer synthesized current evidence on tinnitus mechanisms, integrating peripheral cochlear injury/deafferentation and central maladaptive plasticity models. It highlights roles for increased central gain, thalamocortical dysrhythmia, limbic/salience network modulation, and contributors to chronicity such as neuroinflammation and stress. Clinically, the review emphasizes heterogeneous symptom expression and common comorbidities (e.g., hearing loss and anxiety), guiding mechanistically informed approaches to tinnitus management.

Vanneste S, De Ridder D, Gallus S et al. · Nature reviews. Disease primers · (2026) · View on PubMed ↗

The oscillatory biology of sleep: Linkage to dementia.

This Science perspective examined how sleep-associated coordination of neuromodulators relates to dementia risk and pathology. It describes synchronized ~50-second oscillations in norepinephrine, acetylcholine, serotonin, and dopamine during sleep that are coupled to cerebrospinal fluid flow and linked to glymphatic clearance of metabolic waste. Disruption of neuromodulator signaling during sleep may therefore contribute to neurodegenerative processes relevant to dementia.

Nedergaard M · Science (New York, N.Y.) · (2026) · View on PubMed ↗

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Psychiatry, Stress & Sleep Circuits (depression, anxiety, PTSD/iRBD genetics, sleep mechanisms)

The Evolving Pharmacological Landscape for Paediatric and Adult ADHD.

This review summarized randomized controlled trials of ADHD pharmacotherapies in pediatric and adult populations, focusing on agents not approved for ADHD or used off-label based on trial evidence. It highlights that while stimulants remain highly effective, tolerability and response limitations drive ongoing evaluation of alternative compounds across age groups. Clinically, the synthesis supports more informed selection and future trial design for non-stimulant or repurposed options in ADHD when standard treatments fail.

Fusetto Veronesi G, Tarantino F, Pirolo D et al. · CNS drugs · (2026) · View on PubMed ↗

Dysesthesia associated with GLP-1 agonist therapies: data-mining analysis and literature review.

This study tested the role of G protein-coupled receptor 75 (GPR75) in depression-like behavior and HPA-axis hyperactivity using chronic social defeat stress (CSDS) in mice and postmortem human depression brain analyses. GPR75 was upregulated in arcuate nucleus glutamatergic (ARCVglut2) neurons in susceptible mice, and conditional or local knockout of GPR75 in these neurons produced robust antidepressant-like effects. The findings are significant because they identify a specific excitatory arcuate-paraventricular nucleus circuit mechanism that could be targeted for depression therapeutics.

Laroche ML, Géniaux H, Jardou M · European journal of clinical pharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Genetic associations between post-traumatic stress disorder and REM-sleep behavior disorder.

The study assessed genetic associations between post-traumatic stress disorder (PTSD) and isolated/idiopathic REM sleep behavior disorder (iRBD) using polygenic risk scores (PRS), genetic correlation, and Mendelian randomization, and examined dopamine transporter imaging in iRBD patients stratified by PTSD status. Genetic analyses did not support a causal relationship between PTSD and iRBD, and dopamine transporter imaging was evaluated in small iRBD subgroups (N=6 with PTSD, N=32 without). These results refine the genetic/causal landscape linking PTSD to α-synuclein–related neurodegeneration risk phenotypes such as iRBD.

Ghamgosar Shahkhali M, Liu L, Ghamgosar Shahkhali MH et al. · NPJ Parkinson’s disease · (2026) · View on PubMed ↗ · Free PDF ↗

Updated trends in the global prevalence and burden of mental disorders, 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023.

This systematic analysis of the Global Burden of Disease Study 2023 quantified global trends in prevalence, incidence, and health burden for 12 mental disorders across 21 regions, 204 countries/territories, sexes, and age groups from 1990–2023. The key finding is the updated characterization of how mental disorder burden has changed over time and differs by demographic and socio-demographic index (SDI) strata. Clinically, these results provide evidence to guide public health planning and resource allocation for mental health interventions worldwide.

Lancet (London, England) · (2026) · View on PubMed ↗

Slow-wave sleep engages brainstem circuitry to prevent stress-induced anxiety.

This study examined how slow-wave sleep (SWS) prevents stress-induced anxiety by identifying a GABAergic brainstem circuit from the parafacial zone (PZ) to the lateral parabrachial nucleus (LPB) projecting to the oval bed nucleus of the stria terminalis (ovBNST). The key finding is that optogenetic activation of PZ GABAergic neurons after social defeat stress induces time-locked SWS and prevents anxiety, with multi-region Ca2+ recordings showing suppressed LPB and ovBNST activity during SWS and pathway requirement for anxiolysis. Scientifically, it defines a specific neural circuit node (LPB–ovBNST) through which SWS drives anxiolytic effects, suggesting mechanistic targets for anxiety disorders.

Feng X, Le T, Liu B et al. · Neuron · (2026) · View on PubMed ↗

Reward magnitude determines reinforcement learning efficiency.

This Science study tested in naïve mice how reward magnitude affects reinforcement learning efficiency across five behavioral paradigms. Larger rewards improved learning efficiency via separable effects on within- and across-session learning and task engagement, with ventral striatal dopamine release scaling with reward size and optogenetic dopamine enhancement partially reproducing the benefits. The results indicate that dopamine dynamics and reward magnitude jointly tune learning, informing models of reinforcement and potential interventions for learning-related dysfunction.

Gong S, Martell A, Dudman JT et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Therapeutics & Clinical Trials (solid tumors, CAR T/immune therapies, ADCs, radiotherapy, consensus/guidelines)

International Consensus on Severe Lung Cancer-The Second Edition.

This article presents an International Consensus update on severe lung cancer, focusing on patients with poor performance status (PS 2–4) and incorporating new evidence on therapies, interventional techniques, and supportive care. It synthesizes recommendations from a multidisciplinary expert panel based on a comprehensive review of current literature and emerging real-world data. The consensus is clinically significant because it standardizes management approaches for a high-need subgroup of severe lung cancer patients.

Lin X, Chu Q, Dong Y et al. · Translational lung cancer research · (2026) · View on PubMed ↗ · Free PDF ↗

Assessing the Validity and Acceptability of an Adult Quality of Life Questionnaire, the EORTC QLQ-C30, for Adolescents With Cancer.

This study evaluated the validity, reliability, acceptability, and delivery preferences of the adult cancer quality-of-life instrument EORTC QLQ-C30 in adolescents aged 12–17 years with cancer across languages and cultural backgrounds. It found that the questionnaire’s suitability for adolescents could be assessed in terms of psychometric performance and practical acceptability for this age group. Clinically, the results inform whether and how QLQ-C30 can be used in adolescent oncology trials where patient-reported outcomes are needed.

Sodergren SC, Riedl D, Hossain J et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗

ALG1-mediated PDL1 glycosylation drives macrophage m2 polarization to promote bladder cancer progression.

This study investigated how ALG1-mediated N-glycosylation affects immune regulation in bladder cancer by combining multi-omics analyses with biochemical validation of ALG1–PDL1 interactions. The key finding is that ALG1 directly interacts with PDL1 and catalyzes its glycosylation, and this glycosylation promotes macrophage M2 polarization to drive bladder cancer progression. Clinically, it links a specific glycosylation enzyme (ALG1) to an immune-evasion mechanism (PDL1 glycosylation and M2 polarization), highlighting ALG1/PDL1 glycosylation as a potential therapeutic target.

Zhao JG, Chen ZY, Pan HQ et al. · Cell death and differentiation · (2026) · View on PubMed ↗

Filamin-ETV4/5 acts as mechanosensor-mechanotransducer axis that drives cell competition-mediated elimination of transformed cells.

This study examined how epithelial “winner” cells sense and eliminate transformed “loser” cells during cell competition by identifying a mechanosensor–mechanotransducer axis using a synNotch-based transcriptomic screen. The key finding is that filamin acts as a mechanosensor linking actin remodeling to an ETV4/5–PRKG2 pathway that drives extrusion of oncogenically transformed cells, with transformed cells increasing volume and membrane stretching that is sensed by adjacent normal cells. These results mechanistically connect mechanotransduction to tumor-cell elimination, offering potential targets to modulate cell competition in cancer prevention or therapy.

Wen J, Sai K, Masutani S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Macrophage ALDH2 drives immunotherapy resistance by silencing CXCL9 through metabolic-epigenetic crosstalk.

The authors studied tumor-associated macrophages (TAMs) in immunotherapy-resistant cancer and identified aldehyde dehydrogenase 2 (ALDH2) as a marker of a resistant TAM state, using myeloid-restricted ALDH2 ablation to test effects on immune checkpoint blockade (ICB) response. ALDH2 deficiency increased reactive aldehydes (notably 4-hydroxynonenal), activated PI3K–AKT signaling, and mechanistically silenced CXCL9, thereby promoting immunotherapy resistance. This metabolic-epigenetic crosstalk links ALDH2-driven aldehyde metabolism to CXCL9 regulation and provides a potential target to overcome ICB resistance.

Fang H, Sun J, Xiao Q et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Fulvestrant versus capecitabine as maintenance therapy in hormone receptor-positive, HER2-negative metastatic breast cancer after first-line chemotherapy (FAMILY): a multicenter, open-label, randomized, phase 3 trial.

This multicenter, open-label randomized phase 3 trial studied maintenance therapy with fulvestrant versus capecitabine in hormone receptor-positive, HER2-negative metastatic breast cancer patients after first-line chemotherapy response/control, enrolling 210 patients across 22 hospitals in mainland China. The key finding was the comparative efficacy and safety of the two maintenance strategies using investigator-assessed progression-free survival (PFS) as the primary endpoint (with results reported in the full text). Clinically, the trial addresses which endocrine-based versus chemotherapy maintenance approach best prolongs remission and informs treatment selection for HR+/HER2− metastatic disease.

Wu W, Yang Y, Chen H et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Salvage Radiotherapy Confers an Overall Survival Advantage in Biochemical Recurrence of Prostate Cancer: Evidence from the International PROMISE Registry.

This study analyzed the impact of salvage radiotherapy (SRT) on overall survival in prostate cancer patients with biochemical recurrence (BCR) after prostatectomy using the international PROMISE registry (NCT06320223; 1410 patients). The key finding was that SRT was associated with an overall survival advantage, with restaging at BCR incorporating serologic markers and molecular imaging (PET/CT or PET/MRI) to assign molecular imaging TNM stage. Scientifically and clinically, it strengthens evidence for SRT benefit in BCR and highlights the value of molecular imaging–based staging for outcome interpretation.

Guberina N, Karpinski MJ, Guberina M et al. · Journal of nuclear medicine : official publication, Society of Nuclear Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

ERS/ESGE/ESTS clinical practice guidelines on endobronchial and oesophageal endosonography for the diagnosis and staging of lung cancer.

This guideline article developed ERS/ESGE/ESTS recommendations on endobronchial and oesophageal endosonography for lung cancer diagnosis and staging, focusing on EBUS-TBNA (EBUS via major airways) and EUS-FNA (including EUS performed with an EBUS scope as EUS-B-FNA). The key finding is the synthesis of evidence and GRADE-based recommendations addressing when and how these endosonographic techniques should be used for tissue sampling and staging. Clinically, it standardizes diagnostic pathways to improve staging accuracy and treatment selection in lung cancer.

Korevaar DA, Kovacevic B, Papadopoulou E et al. · The European respiratory journal · (2026) · View on PubMed ↗

Datopotamab deruxtecan (Dato-DXd) in combination with durvalumab as first-line treatment for unresectable locally advanced or metastatic triple-negative breast cancer: results from arms 7 and 8 of the phase Ib/II BEGONIA study.

The phase Ib/II BEGONIA study evaluated datopotamab deruxtecan (Dato-DXd), a TROP2-directed antibody-drug conjugate, combined with durvalumab (anti–PD-L1) as first-line therapy in patients with unresectable locally advanced or metastatic triple-negative breast cancer (TNBC), including arms 7 (all-comers) and 8 (PD-L1–high by local IHC). The abstract indicates arm 8 restricted enrollment to PD-L1–high tumors while arm 7 included patients regardless of PD-L1 status, with efficacy and safety results reported for these combination arms. This trial is clinically significant because it tests a targeted ADC–checkpoint inhibitor regimen (TROP2-Dato-DXd plus durvalumab) for a high-need TNBC population stratified by PD-L1 expression.

Schmid P, Wang HC, Lynce F et al. · Annals of oncology : official journal of the European Society for Medical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Endocytic evasion confers resistance to antibody-drug conjugates therapy in cancer.

This study investigated resistance to the NECTIN4-targeting antibody-drug conjugate enfortumab vedotin (NECTIN4-ADC) in urothelial carcinoma using paired spatial transcriptomics (pre- vs post-NECTIN4-ADC plus anti-PD1), humanized mouse models, single-cell RNA sequencing, and resistant cell systems. It found a resistant tumor-cell population with increased NECTIN4 expression but defective ADC uptake, and mechanistically implicated AKR1C1 binding to NECTIN4 that impairs AP2M1-dependent clathrin-mediated internalization. These findings explain a key endocytic evasion route to NECTIN4-ADC failure and suggest that targeting the uptake machinery or AKR1C1–NECTIN4 axis could improve durability of ADC therapy.

Wang Y, Chen Z, Wang W et al. · Cancer cell · (2026) · View on PubMed ↗

Concurrent genetic and non-genetic resistance mechanisms to KRAS inhibition in colorectal cancer.

This work studied mechanisms of acquired resistance to KRAS inhibition in colorectal cancer by analyzing patient-matched CRC biopsies after combined treatment with the KRASG12C inhibitor and an EGFR inhibitor using targeted exome sequencing and spatial transcriptomics. It showed that most patients develop acquired genetic alterations at progression, but these are often subclonal and coexist with transcriptional adaptive states, with mesenchymal, YAP, and fetal-like signatures predominating in resistant tumors and inflammatory programs induced early. The results clarify that KRAS inhibitor resistance is driven by both genetic and non-genetic (state-switching) programs, informing combination strategies that block adaptive transcriptional routes.

Alonso S, Chu K, Granowsky E et al. · Cancer cell · (2026) · View on PubMed ↗

Lenvatinib plus pembrolizumab in participants with advanced or recurrent endometrial cancer: Study 309/KEYNOTE-775 and ENGOT-en9/LEAP-001 post-(neo)adjuvant therapy outcomes.

This analysis studied outcomes in participants with advanced or recurrent endometrial cancer who received only neoadjuvant, adjuvant, or neoadjuvant-plus-adjuvant platinum-based chemotherapy before enrollment in phase 3 Study 309/KEYNOTE-775 and ENGOT-en9/LEAP-001. The key finding (as reported for this subgroup) is the post-(neo)adjuvant treatment outcome profile for these chemotherapy-pretreated cohorts within the lenvatinib plus pembrolizumab trial framework. Clinically, it refines how prior platinum timing and exposure relate to efficacy and supports more precise interpretation of lenvatinib–pembrolizumab benefit in real-world treatment sequences.

Marth C, Lorusso D, Bidziński M et al. · International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · (2026) · View on PubMed ↗

LDHA-mediated CREB1 Lactylation Promotes Breast Cancer Brain Metastasis by Transcriptionally Activating Cytoskeletal Remodeling.

This study investigated how LDHA-mediated CREB1 lactylation promotes breast cancer brain metastasis using single-cell RNA sequencing (scRNA-seq) of primary tumors and brain metastases. Using five GEO scRNA-seq datasets with clustering, inferCNV, and pseudotime analyses, it identified high-risk malignant sub-clusters and evolutionary states linked to brain metastatic potential and implicated an LDHA–CREB1 lactylation transcriptional program that drives cytoskeletal remodeling. The findings provide a mechanistic target (LDHA/CREB1 lactylation) for developing therapies to prevent or treat brain metastasis in breast cancer.

Liu S, Bai Z, Qiao Y et al. · Neuro-oncology · (2026) · View on PubMed ↗

Multi-Transcriptomics Analysis Identifies NNAT as a Key Molecule Driving the Invasive Phenotype Across All Lineages of Pituitary Adenomas.

This study analyzed pituitary adenoma invasion across lineages using 216 whole-transcriptome sequencing datasets and additional single-cell transcriptomic data to identify drivers of invasive behavior. It identified NNAT as a key molecule associated with the invasive phenotype across all lineages, supporting a transcriptional basis for invasion despite histologic benignity. Scientifically, NNAT emerges as a candidate therapeutic target and biomarker for stratifying invasive pituitary adenomas where targeted options are currently limited.

Liu M, Wang H, Guo J et al. · Neuro-oncology · (2026) · View on PubMed ↗

Patient-reported time toxicity with bispecific antibody therapies in relapsed/refractory follicular lymphoma and diffuse large B-cell lymphoma.

This survey study examined patient-reported time toxicity with bispecific antibodies—mosunetuzumab, glofitamab, and epcoritamab—in relapsed/refractory follicular lymphoma and diffuse large B-cell lymphoma. Among 120 patients (60 FL and 60 DLBCL), participants reported healthcare visit frequency and time spent on treatment administration, travel, recovery, and daily-life impact over the prior 30 days, providing real-world preference and burden data. The results are clinically significant because they quantify the patient-centered time burden of BsAb therapy and can inform shared decision-making and supportive care planning.

Major A, Ma E, Masaquel A et al. · The oncologist · (2026) · View on PubMed ↗ · Free PDF ↗

CSF1R-dependent CD169-positive macrophages locally constrain melanoma growth in the skin.

This study investigated how CSF1R-dependent CD169-positive macrophages regulate melanoma growth in the skin using mouse models, including a syngeneic melanoma system and intravital imaging. It found that CD169+ macrophages in the hypodermis encapsulate and directly suppress melanoma growth, and that CSF1R blockade depletes these macrophages and leads to unrestrained tumor growth independent of B or T cells. These results identify a local, macrophage-mediated tumor containment mechanism in skin and suggest that preserving or harnessing CD169+ macrophage function could be a strategy to improve melanoma control.

Keith YH, Duchini E, Lin X et al. · The Journal of experimental medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Bladder Adjuvant Radiotherapy: Phase III Multicenter Randomized Controlled Trial of Adjuvant Radiotherapy or Observation for Postcystectomy Muscle-Invasive Bladder Cancer.

This phase III multicenter randomized controlled trial studied whether adjuvant radiotherapy (stoma-sparing IG-IMRT 50.4 Gy/28 fractions) versus observation improves 2-year locoregional recurrence-free survival in high-risk nonmetastatic muscle-invasive bladder cancer patients after chemotherapy and radical cystectomy. Adjuvant RT was tested in patients meeting high-risk criteria (e.g., T3-4, N1-3, margin positive, or ≤10 nodes dissected) and stratified by nodal involvement and chemotherapy type. If effective, this approach would refine post-cystectomy management by adding targeted pelvic nodal/cystectomy-bed irradiation to reduce locoregional recurrence in high-risk patients.

Murthy V, Maitre P, Pal M et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Multiomic analyses delineate human neuroendocrine tumor cell states in relation to normal enteroendocrine cell ontogeny.

This study used multiomic profiling to map human small intestine neuroendocrine tumor (SI-NET) cell states relative to normal enteroendocrine cell ontogeny, focusing on transcriptional programs involving ASCL1 and NEUROD1. SI-NETs resembled mature enterochromaffin cells but individual tumor cells co-expressed stem/progenitor genes, indicating a hybrid differentiation state linked to normal enteroendocrine developmental timing. These data refine the developmental model of SI-NET biology and may identify differentiation-state vulnerabilities for future targeting.

Singh PN, Hadj Bachir E, Howe JR et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

Anti-BCMA/GPRC5D CAR T in relapsed or refractory multiple myeloma patients with extraosseous extramedullary disease.

This single-arm, open-label phase 2 trial evaluated anti-BCMA/GPRC5D bispecific CAR T cells in 37 relapsed or refractory multiple myeloma (RRMM) patients with extraosseous extramedullary disease (EMD). At a median follow-up of 10.1 months, 36/37 patients (97%) achieved overall response and measurable residual disease (MRD) negativity, with 16 (43%) achieving the truncated outcome category reported in the abstract. The results support further development of anti-BCMA/GPRC5D CAR T therapy as a potentially effective option for RRMM patients with otherwise poor outcomes due to extraosseous EMD.

Zhou D, Qi Y, Ma S et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

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Hematologic Malignancies & Transplant/Cell Therapy (AML/ALL, myeloma MRD, CAR T, clonal hematopoiesis)

Co-occurring clonal hematopoiesis exhibits strong selection and high leukemia risk.

The study analyzed genomic data from 546,090 biobank participants to quantify how co-occurring clonal hematopoiesis (CHIP) and mosaic chromosomal alterations (mCAs) behave, using selection/enrichment metrics and leukemia risk assessment. Co-occurring CH (≥2 CH mutations) was present in 1.6% of cancer-free individuals, showed strong evidence of selection (up to 804× enrichment), and was more common after prior cancer (3.6%), with co-occurrence associated with greater telomere attrition and hematologic disruption. These findings indicate that co-occurring CH represents a highly selected, high-risk clonal state for future leukemia development.

Barnao KM, Hubbard AK, Chan ICC et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Human CART22.19 therapy in refractory pediatric B-ALL: insights from a named-patient cohort.

This named-patient cohort study evaluated Human CART22.19, a fully human tandem CD19/CD22 CAR T-cell therapy, in nine heavily pretreated pediatric patients with relapsed/refractory B-cell acute lymphoblastic leukemia (B-ALL). The key finding was clinical experience showing feasibility and outcomes in a setting where relapse can involve CD19 antigen escape, including patients with CD19-negative blast populations. The results provide real-world translational insights into dual-target CAR design aimed at improving persistence and reducing antigen-escape relapse in pediatric B-ALL.

Mast AS, Lang P, Schlegel P et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Peripheral Measurable Residual Disease Activity Assessment by MALDI-TOF Mass Spectrometry in Patients With Newly Diagnosed Multiple Myeloma in the Phase III GMMG-HD7 Trial.

This study evaluated MALDI-TOF mass spectrometry (MS) for peripheral measurable residual disease (MRD) activity detection in 617 newly diagnosed multiple myeloma patients enrolled in the phase III GMMG-HD7 trial (3,301 serum samples). MS reliably distinguished therapeutic antibodies, tracked diagnostic M-proteins longitudinally, and MS negativity was associated with improved progression-free survival, with the strongest prognostic separation at later time points (e.g., 12 months of maintenance). These findings support MS-based, minimally invasive MRD activity assessment as a clinically meaningful prognostic tool in prospective multiple myeloma trials.

Jin JX, Ginde VR, Huhn S et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Venetoclax Plus Pediatric Regimen in Adolescents and Adults with Ph-Negative Acute Lymphoblastic Leukemia.

This prospective phase 2 study evaluated venetoclax combined with pediatric-inspired chemotherapy in 167 adolescents and adults (14–60 years) with newly diagnosed Philadelphia chromosome–negative (Ph−) acute lymphoblastic leukemia (ALL). The complete remission rate was 91.0%, and 73.0% of responders achieved measurable residual disease (MRD) negativity by multiparameter flow cytometry (MFC) after induction, meeting the primary endpoint. These results support venetoclax as a first-line intensification strategy for Ph− ALL with MRD-driven response rates, warranting longer follow-up for survival benefit.

Gong X, Liu Y, Fang Q et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

N6-methyladenosine reader IGF2BP2 in T-cell lymphoma.

This study investigated the role of the m6A reader IGF2BP2 in peripheral T-cell lymphoma (PTCL) using expression analyses across multiple cohorts and functional experiments. IGF2BP2 was consistently highly expressed across common nodal PTCL subtypes in three external cohorts and in an RNA-seq dataset of 196 newly diagnosed PTCL patients, and IGF2BP2 promoted tumor growth while inhibiting CD8+ T-cell infiltration in vitro and in vivo. Mechanistically, IGF2BP2 binding to specific mRNA targets (described in the truncated abstract) supports its potential as a therapeutic biomarker and target in PTCL.

Hu S, Qin Y, Yi HM et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

Prognostic impact of FLT3-ITD microclones in young adults with acute myeloid leukemia treated with intensive chemotherapy.

This post-hoc analysis assessed the prognostic impact of low-level FLT3-ITD microclones in young adults with acute myeloid leukemia (AML) treated with intensive chemotherapy in the BIG-1 trial (NCT02416388). Using next-generation sequencing (NGS), FLT3-ITD microclones (allelic ratio 0.0004–0.05) were detected in 17.4% of patients without FLT3-ITD macroclones and were independently associated with increased relapse risk, similar to macroclones. The results indicate that even low-level FLT3-ITD subclonal architecture has clinical prognostic value and should be considered in risk stratification.

Duployez N, Joudinaud R, Boudry A et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

Chromosome 5q deletion drives evolution of aneuploidy in myeloid neoplasms with complex karyotype.

This study developed a patient-derived induced pluripotent stem cell (iPSC) model to determine how chromosome 5q deletion (del5q) drives aneuploidy evolution in myeloid neoplasms with complex karyotype (AML-CK). Single-cell tracking after transient mitotic inhibition showed that TP53-mutant HSPCs with del5q evolved into distinct highly aneuploid states, implicating del5q as a driver of aneuploid progression beyond TP53 mutation alone. The work provides a mechanistic framework for clonal trajectories in high-risk AML-CK and may inform strategies to target early steps of karyotype evolution.

Creamer JP, Ray S, Stewart S et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

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Immunology & Autoimmunity (immune pathways, CAR for autoimmunity, FcRn/MG overshoot, Behçet T2T)

Anti-acetylcholine receptor antibody overshoot following efgartigimod in myasthenia gravis: Two case reports with literature review.

These case reports described anti-acetylcholine receptor (AChR) antibody overshoot and clinical worsening after treatment with the FcRn antagonist efgartigimod in patients with generalized myasthenia gravis, supplemented by a literature review of previously reported overshoot cases. The key finding was that efgartigimod can precipitate a paradoxical rise (“overshoot”) in AChR antibodies shortly after FcRn blockade, potentially exacerbating MG symptoms. This is clinically significant because it underscores the need for monitoring and management strategies for antibody overshoot when using FcRn-targeted therapy.

Yang RY, Wang BR, Hong Y et al. · Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · (2026) · View on PubMed ↗

Treat-to-target in Behçet syndrome.

This review evaluated the treat-to-target (T2T) strategy in Behçet syndrome, integrating evidence from clinical trials and expert consensus to define how T2T could be operationalized in this heterogeneous disease. The key finding is that, despite limited direct T2T literature, trial-based advances support adopting a structured T2T approach in Behçet syndrome. Clinically, it provides an evidence-based framework to improve disease control and standardize outcomes across multidisciplinary care.

Bettiol A, Bertsias G, Bodaghi B et al. · Nature reviews. Rheumatology · (2026) · View on PubMed ↗

Resetting autoimmune disease with CAR cell therapies.

This Nature Medicine review surveyed how CAR cell therapies can “reset” autoimmune disease by selectively depleting pathogenic B cells, focusing on current technologies and key targets. The key finding is that deep B-cell depletion using CAR T or related CAR platforms (notably targeting CD19 and B-cell maturation antigen) is a promising strategy to reprogram immune responses in autoimmune diseases. Clinically, it frames unmet needs—such as safety, durability, and target selection—and positions CAR approaches as an emerging disease-modifying option for autoimmune conditions.

Schett G, Xu H · Nature medicine · (2026) · View on PubMed ↗

IRAK2 deficiency causes immune dysregulation through defective Myddosome assembly and enhanced interferon responses.

This study investigated the consequences of IRAK2 deficiency in humans by characterizing twelve patients with homozygous loss-of-function IRAK2 copy-number variants (IRAK2-∆ex2) and assessing downstream innate immune signaling. The IRAK2-∆ex2 protein failed to interact with IRAK4, causing defective Myddosome assembly and impaired NF-κB activation, alongside enhanced type I interferon responses that manifested as recurrent infections, autoantibodies, and gastrointestinal ulceration. These results define a mechanistic cause of immune dysregulation in IRAK2-related primary immunodeficiency/autoimmunity and clarify how Myddosome signaling controls interferon balance.

Fei Y, Liu L, Ma S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

One-Year Clinical Remission with Tezepelumab in Severe Asthma: TERESA Single-Arm Prospective Study.

This prospective multicenter single-arm phase 4 study (TERESA) evaluated tezepelumab, an anti–thymic stromal lymphopoietin (TSLP) monoclonal antibody, in patients with uncontrolled severe asthma to assess clinical remission at week 52, including biologic-experienced participants. The key finding was the achievement of one-year clinical remission with tezepelumab in this severe asthma population (reported as the study’s primary outcome). The results support tezepelumab as a disease-modifying option aimed at sustained remission rather than only symptom control in severe asthma.

Kan-O K, Watanabe H, Chibana K et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

TL1A as a therapeutic renaissance in inflammatory bowel disease: a systematic review from molecular mechanisms to clinical translation.

This systematic review evaluated TL1A (TNF-like cytokine 1A) and its death-domain receptor 3 (DR3) signaling pathway as therapeutic targets in inflammatory bowel disease, spanning molecular mechanisms through clinical translation. It summarizes evidence for TL1A/DR3 biology and critically assesses TL1A-targeted interventions, emphasizing unmet needs in IBD such as inadequate response and lack of agents addressing fibrosis and barrier dysfunction. The review is significant because it frames TL1A as a potential “therapeutic renaissance” target and outlines how future precision-medicine approaches could select patients most likely to benefit.

Liang RF, Pugliano CL, Hughes R et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

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Infectious Disease & Antivirals (HBV entry, antiviral defense mechanisms, Ebola outbreak)

Scavenger receptor class F member 2 is an intracellular receptor for hepatitis B virus.

The authors investigated hepatitis B virus (HBV) entry and intracellular trafficking by testing whether scavenger receptor class F member 2 (SCARF2) functions as an intracellular receptor for HBV in addition to the known NTCP/preS1 interaction. They report that SCARF2 binds a preS1 region downstream of the NTCP binding site via its N-terminal EGF-like domains 4–6, with the proline-rich C-terminal domain also required for infection, and that internalized virions depend on this mechanism. This is clinically significant because it expands the HBV entry receptor framework and highlights SCARF2 as a potential antiviral target.

Li C, Wang Y, Xiong R et al. · Cell · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Alphaviral non-structural protein-host RBP co-condensation as a mechanism to sustain virus replication.

This study investigated how alphavirus non-structural protein nsP3 uses host RNA-binding proteins (RBPs) to sustain viral replication, using Semliki Forest virus (SFV) as a model. The key finding is that nsP3 exploits G3BP to drive nsP3–G3BP co-condensation, converting antiviral stress granules into proviral co-condensates that protect viral genomic RNA from RNase degradation and promote viral translation and replication. Scientifically and therapeutically, it suggests that disrupting nsP3–G3BP co-condensation or related RBP interactions could be an antiviral strategy.

Liu Y, Yao Z, Zhang Y et al. · Molecular cell · (2026) · 1 citations · View on PubMed ↗

Scientists play catch-up to startling Ebola outbreak.

This Science news piece described how scientific and public-health efforts are ramping up during the Ebola outbreak involving Bundibugyo virus as it spreads. It highlights accelerated testing, sequencing, and clinical trial development to keep pace with transmission. Rapid diagnostics and trial initiation are crucial for improving outbreak control and treatment options in real time.

Kupferschmidt K · Science (New York, N.Y.) · (2026) · View on PubMed ↗

DNA polymerization activates RNA cleavage of a reverse transcriptase-like antiviral enzyme.

This mechanistic study investigated how a defense-associated reverse transcriptase-like enzyme, DRT4, uses DNA polymerization to activate RNA cleavage during antiviral defense in the context of phage infection. DRT4 integrates DNA polymerase, exonuclease, and RNA endonuclease activities, where elevated dNTPs shift the polymerase–exonuclease equilibrium to promote protein-primed ssDNA synthesis that then activates RNA cleavage. The findings clarify a ncRNA-independent DRT4 activation pathway, advancing understanding of programmable antiviral defense mechanisms.

Rong X, Xiao J, Zhao X et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

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Cardiovascular Disease (heart failure, hypertrophy, atherosclerosis, PAH, vascular remodeling, eosinophilic heart disease)

SREBP1 Transactivation of NHE3 Impairs Cardiac Contraction and Aggravates Heart Failure.

This study investigated the role of the metabolic transcription factor SREBP1 in heart failure with reduced ejection fraction (HFrEF) by analyzing cardiac tissues from HFrEF patients and mice subjected to transverse aortic constriction (TAC), focusing on SREBP1 transactivation of the Na+/H+ exchanger NHE3. It found that SREBP1-driven NHE3 dysregulation impairs cardiac contraction and worsens HFrEF phenotypes. Scientifically, the work links SREBP1 to pathological ion handling via NHE3, suggesting a potential therapeutic axis for improving contractility in HFrEF.

Gu H, Wen J, Liu Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗

Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation.

This study examined whether the RNA-binding protein Sam68 (KHDRBS1) drives pathologic cardiac hypertrophy by suppressing cardiomyocyte glucose oxidation, using failing human heart data, transcriptomic analyses, and cardiomyocyte-specific Sam68 knockout (Sam68cKO) mice. It reports that Sam68 exacerbates hypertrophy and that loss of cardiomyocyte Sam68 improves metabolic glucose oxidation, thereby mitigating maladaptive remodeling. The findings identify Sam68 as a mechanistic regulator connecting stress signaling to impaired myocardial energy metabolism in pathologic hypertrophy.

An J, Han C, Jiang Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗

Empagliflozin restores cardiac function in obese-diabetic HFpEF mice but further alters gene expression.

This study tested whether in vivo treatment with the SGLT2 inhibitor empagliflozin improves excitation–contraction coupling, electrophysiology, and gene transcription in a translational two-hit HFpEF mouse model combining obese-diabetic leptin receptor–deficient db/db mice with chronic aldosterone infusion (db/db+Aldo). Empagliflozin restored cardiac function and further altered cardiac gene expression, despite the near absence of SGLT2 in cardiomyocytes, suggesting a cardioprotective mechanism beyond direct cardiomyocyte SGLT2 signaling. These findings support a mechanistic basis for SGLT2 inhibitor benefit in HFpEF and motivate further work to define the downstream gene programs and ECC targets involved.

Mira Hernandez J, Bailey LRJ, Salemme VR et al. · Basic research in cardiology · (2026) · View on PubMed ↗ · Free PDF ↗

Flow-mediated endothelial remodeling and inflammation drive developmental vascular susceptibility in ldlr loss of function.

The study used low-density lipoprotein receptor loss-of-function zebrafish (ldlr-/-) to test how developmental flow-mediated endothelial remodeling and inflammation create susceptibility to atherosclerosis, applying single-cell RNA sequencing under differential flow conditions. It identified a population of disproportionately stressed endothelial cells with heat-shock program activation and linked developmental endothelial stress/inflammation to later vascular disease susceptibility. These findings connect monogenic LDLR loss-of-function with developmental hemodynamic programming of endothelial inflammation, offering mechanistic targets for early prevention.

Kaveh A, Salazar-Martin AG, Dai W et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondria-derived vesicles with bioenergetic units from brown adipose tissue attenuate cardiac remodeling post-myocardial infarction.

The authors investigated whether mitochondria-derived vesicles (MDVs) from brown adipose tissue (BAT) influence cardiac remodeling after myocardial infarction, focusing on vesicle transfer to cardiac macrophages. They found that BAT-derived MDVs attenuated post-MI pathological remodeling through anti-inflammatory effects, with mitochondrial membrane-containing vesicles mobilizing to the heart under stress and VPS35 translocation to mitochondria driving protein packaging into MDVs. This identifies a specific inter-organ vesicle-mediated mechanism by which BAT can protect the heart and modulate macrophage-driven remodeling.

Shi T, Chen F, Xu Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Three-dimensional micro-CT analysis of vascular remodeling and vascular pruning in pulmonary arterial hypertension.

This study used three-dimensional micro-computed tomography (µCT) to quantify pulmonary vascular remodeling and vascular pruning in pulmonary arterial hypertension (PAH) using explanted lungs from patients and healthy controls. In end-stage idiopathic or heritable PAH lungs, µCT enabled detailed measurement of arterial lumen dimensions and related vascular alterations, providing quantitative characterization of pruning/remodeling features. The approach offers a high-resolution imaging framework to better phenotype PAH and potentially track disease mechanisms and progression.

Aerts G, Willems L, Tielemans B et al. · The European respiratory journal · (2026) · View on PubMed ↗

Current state of knowledge on the epidemiology, aetiology, diagnosis, and management of heart involvement in eosinophilia. A Clinical Consensus Statement of the ESC Working Group on Myocardial & Pericardial Diseases.

This European Society of Cardiology (ESC) clinical consensus statement reviewed the epidemiology, etiology, diagnosis, and management of heart involvement in eosinophilia, focusing on eosinophilic heart disease. It emphasizes that peripheral eosinophilia may be absent in some patients and that biopsy of the affected tissue is often essential for correct diagnosis, particularly in advanced or atypical presentations. The consensus aims to improve early recognition and management of a rare but high-morbidity cardiac condition associated with eosinophilia.

Kuchynka P, Brucato A, Tschöpe C et al. · European journal of heart failure · (2026) · View on PubMed ↗

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Metabolism, Obesity & Liver Disease (GLP-1/tirzepatide, MASLD/MASH, lipotoxicity, exercise exerkines)

MASLD prevalence, incidence and global aspects.

This review assessed the global epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD), summarizing estimates of prevalence, incidence, disability from complications, and reduced life expectancy across populations. It emphasizes that MASLD burden is tightly linked to global obesity and type 2 diabetes epidemics and that prevalence estimates vary substantially by population (including differences across sub-Saharan Africa). Scientifically and clinically, the synthesis clarifies the scale and heterogeneity of MASLD risk to inform screening, prevention, and health-system planning worldwide.

Wild SH, Lazarus JV, Spearman CW et al. · Diabetologia · (2026) · View on PubMed ↗ · Free PDF ↗

Causes and consequences of discontinuation of GLP1RAs or tirzepatide.

This review analyzed real-world persistence and discontinuation patterns for GLP-1 receptor agonists and tirzepatide in type 2 diabetes mellitus and obesity, focusing on causes of stopping therapy. It reports that persistence is often suboptimal, with many patients discontinuing within the first year, commonly due to gastrointestinal adverse effects, insufficient efficacy, and cost-related barriers. The clinical significance is that understanding discontinuation drivers can guide patient counseling, side-effect management, and selection of alternative strategies to improve long-term outcomes.

Ceriello A, Prattichizzo F, Mastan Sheik Abdullah AR et al. · Nature reviews. Endocrinology · (2026) · View on PubMed ↗

G protein-coupled receptor 75 mediates depression-like behaviors and HPA axis hyperactivity through an excitatory arcuate-paraventricular nucleus circuit.

This pharmacovigilance study used VigiBase disproportionality analysis to characterize dysesthesia (especially burning skin sensations) associated with GLP-1 receptor agonists and tirzepatide, using the HLT “Paraesthesia and dysesthesia” and information component (IC) metrics. The key finding was that reports of dysesthesia were detectable as a signal in association with GLP-1R agonists/tirzepatide, and the authors complemented the signal with a narrative review of French pharmacovigilance case reports. This is significant for clinicians because it highlights a potentially underrecognized adverse effect and supports improved recognition and reporting of sensory symptoms during GLP-1 therapy.

Wang H, Wei YH, Gao AQ et al. · Acta pharmacologica Sinica · (2026) · View on PubMed ↗

Blocking MOXD1-derived ACOX1 peroxisome trafficking suppresses metabolic dysfunction-associated steatohepatitis.

This study investigated regulators of hepatic lipotoxicity driving metabolic dysfunction-associated steatohepatitis (MASH) by integrating murine and human MASH RNA-seq datasets and then performing mechanistic and functional experiments. It found that blocking MOXD1-derived ACOX1 peroxisome trafficking suppresses metabolic dysfunction-associated steatohepatitis, implicating the MOXD1–ACOX1 trafficking axis in disease progression. The work suggests a tractable therapeutic target in MASH by interfering with peroxisomal lipid-handling pathways.

Li M, Zhang J, Yang Y et al. · Gut · (2026) · View on PubMed ↗

The Paradox and Future of GLP-1/GIP Combination Therapies: Efficacy and Mechanisms.

This review analyzed the efficacy and mechanistic basis of GLP-1 receptor (GLP-1R)–based obesity pharmacotherapies, focusing on marketed and investigational GLP-1R agonists such as semaglutide and the GLP-1/GIP dual agonist tirzepatide, as well as the GLP-1RA/GIP antagonist maridebart cafraglutide. It highlights that both GLP-1R/GIPR dual targeting strategies can yield beneficial metabolic effects, while noting limited human evidence for anorectic effects from GIPR agonism or antagonism alone. The synthesis informs future obesity drug development by clarifying how GLP-1R and GIPR modulation may contribute to metabolic outcomes beyond appetite alone.

Davies I, Holst JJ, Rosenkilde MM et al. · Annual review of nutrition · (2026) · View on PubMed ↗

Semaglutide-associated risk of nonarteritic anterior ischemic optic neuropathy in patients with type 2 diabetes: A systematic review and meta-analysis of observational studies.

This systematic review and meta-analysis evaluated whether semaglutide, a GLP-1 receptor agonist, is associated with increased risk of nonarteritic anterior ischemic optic neuropathy (NAION) in patients with type 2 diabetes (T2DM). Across observational studies comparing semaglutide users with users of other glucose-lowering therapies, the analysis assessed NAION incidence/risk in T2DM populations aged ≥12 years. The study addresses a safety signal from case reports and informs risk-benefit considerations for semaglutide prescribing in T2DM.

Chrzanowski J, Walicka M, Burzyński J et al. · PLoS medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Kidney & Renal Fibrosis/Calcification (CKD fibrosis, kidney fibrosis signaling, vascular calcification in CKD)

The E3 ubiquitin ligase Itch plays an essential role in kidney fibrosis by inhibiting Dvl2/GSK3β/β-catenin signaling pathway.

This study tested the role of the E3 ubiquitin ligase Itch in kidney fibrosis by analyzing human CKD renal tubules and mouse models of unilateral ureteral obstruction (UUO) and folic acid (FA) injury, using Itch knockout (Itch-/-) and Itch overexpression approaches. Itch expression was decreased in diseased renal tubules, and Itch loss worsened fibrosis and inflammation while Itch overexpression alleviated UUO- or FA-induced kidney fibrosis, mechanistically involving inhibition of the Dvl2/GSK3β/β-catenin signaling pathway. These findings identify Itch as a protective regulator of fibrotic signaling and suggest that restoring Itch–Dvl2/GSK3β/β-catenin control could be a therapeutic strategy for CKD progression.

Li Y, Zhang W, Xie Y et al. · Cell death and differentiation · (2026) · View on PubMed ↗

Thoracic perivascular adipose tissue-derived PI16 alleviates vascular calcification via CKAP4/PI3K/Akt pathway.

The authors investigated whether thoracic perivascular adipose tissue (tPVAT) protects against medial arterial calcification using experimental models of CKD-associated calcification (adenine-induced CKD) and vitamin D3-induced calcification, focusing on the CKAP4/PI3K/Akt pathway. They report that tPVAT-derived PI16 alleviates vascular calcification via signaling through CKAP4/PI3K/Akt. This is significant because it identifies a mechanistic, potentially targetable adipose-derived factor (PI16) and pathway for limiting vascular calcification in chronic kidney disease.

Qiu S, Gao W, Wu D et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

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Reproductive Biology & Fertility (oocyte-to-embryo transition, proteostasis)

20S proteasome-regulated proteostasis in ELVAs is critical for oocyte-to-embryo transition and female fertility.

This study investigated how intrinsic proteasome insufficiency in endolysosomal vesicular assemblies (ELVAs) affects oocyte-to-embryo transition (OET) and female fertility using mice with oocyte-specific deletion of a proteasomal core subunit. The key finding is that 20S proteasome-regulated proteostasis within ELVAs is critical for successful OET and for maintaining female fertility. Scientifically, it identifies ELVA-localized 20S proteostasis as a physiological requirement for maternal protein clearance during early development, refining how proteasome biology controls reproductive success.

Rong Y, Chen Y, Cao H et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

Hyocholic acids shape neonatal immune tolerance and microbiota assembly.

This work studied human newborns to determine how hyocholic acid (HCA) species shape neonatal immune tolerance and microbiota assembly, linking bile-acid composition to T-cell differentiation. The key findings are that HCAs (produced via the fetal-specific enzyme CYP3A7) drive CD4+ T cells toward regulatory T cells while suppressing Th17 differentiation, and that neonates with higher HCA levels had reduced infections and gastrointestinal disorders in the first year. This is significant because it identifies a transient, developmentally programmed bile-acid window that may be leveraged to promote early-life immune tolerance and healthy microbiome colonization.

Zheng X, Wang J, Sun Y et al. · Cell metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Genetics, Genomics & Biomarkers (GWAS/PRS, gene curation, multi-omics risk prediction, imaging tracers)

Autoimmune diseases and risk of adverse pregnancy outcomes: a population-based cohort study of five million pregnancies in the UK.

This population-based cohort study evaluated associations between 17 autoimmune diseases and 12 adverse pregnancy outcomes in five million pregnancies from UK primary care practices contributing to the CPRD (2000–2022), linked to Hospital Episode Statistics. Using modified Poisson regression with robust standard errors, it estimated adjusted relative risks for pregnancy outcomes across autoimmune disease exposures. The large-scale evidence is important for counseling and risk stratification of pregnant people with autoimmune conditions.

Singh M, Subramanian A, Wambua S et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Gene-disease relationships for glomerular phenotypes: expert recommendations from ClinGen.

This ClinGen expert recommendation article evaluated evidence standards for curating gene–disease relationships specifically for glomerular phenotypes to determine which gene–variant assertions are robust enough for diagnostic and clinical use. The key finding is the establishment of expert, evidence-based guidance for gene curation in glomerular disease, clarifying how to classify pathogenicity and clinical utility of gene–disease links. Scientifically, it improves consistency and reliability of genetic testing interpretation in nephrology and helps prioritize genes for patient management and future research.

Byrne AB, Li AS, Chung EYM et al. · Nature reviews. Nephrology · (2026) · View on PubMed ↗

Genome-wide association and population-tailored polygenic risk for Parkinson’s disease in Taiwan.

The authors performed a Taiwan population-tailored genome-wide association study using a Taiwanese case-control cohort (2245 Parkinson’s disease cases, 2147 controls) genotyped on the Illumina NeuroBooster Array and imputed with the Taiwan Biobank reference panel. They identified genome-wide significant signals at SNCA and MCCC1, refined the SNCA locus with conditional/joint analyses suggesting an additional 5′ SNCA component, and used locus-focused haplotypes to delineate an East Asian-enriched SNCA risk haplotype. This work improves PD genetic risk prediction and highlights population-specific SNCA architecture relevant for East Asian ancestry.

Chu YT, Su YA, Lin CH et al. · NPJ Parkinson’s disease · (2026) · View on PubMed ↗ · Free PDF ↗

A multi-omics atlas of multisystem complications in type 2 diabetes reveals molecular signatures and improves risk prediction.

This study used multi-omics profiling in UK Biobank participants with type 2 diabetes to build proteomic and metabolomic atlases of 19 T2D-related outcomes and to develop predictive panels using cross-sectional and longitudinal analyses. Key findings (as described in the abstract) were that plasma proteins and metabolites show measurable associations with multiple T2D complications and that machine-learning models can balance predictive performance with clinical feasibility. Scientifically, it provides multi-omics signatures and risk-prediction tools that could improve stratification for multisystem T2D complications.

Zhang H, Yue T, Wang S et al. · Metabolism: clinical and experimental · (2026) · View on PubMed ↗

Supplements and Drugs Are Associated With Biological Age in a Cohort of Exceptionally Healthy Individuals.

This cross-sectional cohort study analyzed 4,260 exceptionally healthy “health enthusiasts” who purchased saliva-based DNA epigenetic tests and completed lifestyle/supplement questionnaires, using a proprietary 9-CpG epigenetic clock (mean absolute error 5.4 years) to measure biological age. It tested associations between 84 commonly used supplements/drugs and biological age (Age Residual) and found that supplement and drug use patterns were linked to biological age metrics in this high-supplement-use population. The work supports the feasibility of studying supplement effects on epigenetic aging in a powered cohort, though causal inference remains limited by the cross-sectional design.

Pabis K, Wang W, Selvarajoo K et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Biallelic loss-of-function mutations in BPNT1 cause vitamin B12-dependent megaloblastic anemia.

This genetic and mechanistic study identified biallelic loss-of-function mutations in BPNT1 as the cause of recurrent vitamin B12-dependent megaloblastic anemia in three affected patients. BPNT1 deficiency led to accumulation of 3′-phosphoadenosine 5′-phosphate (PAP), impaired ribosome biogenesis, and reduced ileal expression of the cubam receptor complex in Bpnt1-null mice. These findings establish BPNT1 as a new disease gene and connect its loss to disrupted intestinal B12 uptake and cellular translation control.

Zeng YH, Li YH, Yuan RY et al. · Blood · (2026) · View on PubMed ↗ · Free PDF ↗

No overall increased risk of death in individuals with sickle cell trait: a study of 467 779 general population adults.

This UK Biobank cohort study examined whether sickle cell trait (SCT), identified by whole-exome sequencing, is associated with mortality and SCT-linked diseases in 467,779 general population adults. Over a median 15-year follow-up, SCT carriers (n=1,253) showed no increased risk of all-cause death (HR 1.04, 95% CI 0.84–1.29) or several outcomes including cardiovascular death, myocardial infarction, ischemic stroke, pulmonary embolism, and heart failure. These findings suggest SCT does not confer a measurable survival disadvantage in the general UK population, informing risk counseling and clinical surveillance strategies.

Warny M, Glenthøj A, Afzal S et al. · Blood · (2026) · View on PubMed ↗

Illuminating proinflammatory myeloid cells with PET tracers targeting GPR84.

This preclinical imaging study developed and validated two fluorine-18 PET tracers, [18F]MGX-110S and [18F]MGX-111S, that target the myeloid activation biomarker GPR84. The tracers were designed to bind specifically to human GPR84-expressing activated myeloid cells (including microglia and macrophages), addressing the lack of specificity in many existing neuroinflammation PET agents. These results support GPR84-targeted PET as a more selective tool for noninvasively monitoring chronic neuroinflammation and myeloid-driven tissue damage in vivo.

Kalita M, Kuo RC, Straniero V 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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Molecular & Cellular Mechanisms (autophagy/lysosomes, membrane nanoclusters, splicing, tRNAome, proteasome, vesicles)

AI-guided redesign of laboratory-evolved reverse transcriptases enhances prime editing.

This study used structure-informed AI-guided protein redesign (ProteinMPNN inverse-folding) to engineer the reverse transcriptase (RT) domains of laboratory-evolved prime editors, testing engineered prime editors in cells. The redesigned RTs carried 30–163 amino-acid substitutions while preserving catalytic regions, improving folding stability, soluble expression, and prime editing performance (up to ~2-fold higher intracellular activity). Scientifically, the work provides a generalizable strategy to decouple prime editor efficiency from protein stability, advancing more robust prime-editing tools for genome engineering.

Tao YA, Sakai HA, Jiang AY et al. · Nature biotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

De novo design of miniproteins targeting GPCRs.

This study developed computational de novo design methods and a high-throughput “receptor diversion” microscopy-based screening pipeline to generate GPCR-binding miniproteins with high affinity, potency, and selectivity. The key finding is that the approach produced functional miniprotein agonists for itch- and pain-related GPCRs and antagonists for GPCRs implicated in cancer, diabetes/obesity, and migraine, with cryo-EM used to support receptor engagement/structure. Clinically and scientifically, it provides a scalable platform for engineering GPCR modulators that could accelerate drug discovery for multiple therapeutic areas.

Muratspahić E, Feldman D, Kim DE et al. · Nature · (2026) · View on PubMed ↗

Allele-specific CRISPR perturbation of the imprinted Dlk1-Dio3 domain reveals regulation of BMP-NOTCH-VEGF signaling in embryonic organogenesis.

This study used allele-specific CRISPR/Cas9 perturbation to insert a transcriptional termination cassette into the imprinted Dlk1-Dio3 domain in mice, generating homozygous (HOMO), maternally inherited (MK), paternally inherited (PK), and wild-type (WT) allele models. The key finding is that parent-of-origin-specific disruption causes allele-specific dysregulation of imprinted genes, altered epigenetic stability at the locus, and downstream changes in BMP–NOTCH–VEGF signaling during embryonic organogenesis, supported by integrative transcriptomics and scRNA-seq at embryonic day 14.5 (E14.5). Scientifically, it provides a precise allele-resolved map of how the Dlk1-Dio3 imprinting control network coordinates multi-organ developmental signaling.

Xing J, Zhang M, Yu H et al. · Cell death and differentiation · (2026) · View on PubMed ↗ · Free PDF ↗

The perijunctional zone is a molecularly distinct muscle subdomain altered in Duchenne muscular dystrophy.

The study characterized the molecular composition of the neuromuscular junction (NMJ) perijunctional zone (PJZ) in mice, using TurboID proximity proteomics targeted to the PJZ via neurofascin (Nfasc) and ankyrin scaffolding. Proximity proteomics identified numerous PJZ-enriched proteins, including Perilipin 4 (Plin4), and showed that the PJZ is a molecularly distinct muscle subdomain altered in Duchenne muscular dystrophy. These findings define PJZ-specific molecular organization and nominate candidate PJZ proteins that may contribute to NMJ dysfunction in Duchenne muscular dystrophy.

Haddix SG, Zhang C, Liu Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Structural basis and physiological significance of non-canonical Gs coupling to the melatonin MT1 receptor.

The authors investigated how the melatonin MT1 receptor (MT1) couples to heterotrimeric G proteins, combining in vitro/in vivo functional assays with a cryo-electron microscopy structure of the melatonin–MT1–Gs complex. They found that MT1, unlike MT2, couples to Gs and activates the Gs/cAMP pathway after long-term melatonin exposure in vivo under dawn-like conditions, with a distinct ligand-binding mode versus the MT1–Gi complex. This structural and physiological mechanism clarifies non-canonical Gs coupling rules for MT1 and informs how circadian melatonin signals can drive different intracellular pathways.

Oishi A, Okamoto HH, Ikegami K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Host mature tRNAome as a decoding switch regulates antiviral and proviral responses.

The study examined how the host mature tRNAome regulates antiviral versus proviral outcomes by coupling tRNA maturation/charging to interferon signaling, using interferon-alpha (IFN-α) to remodel the mature tRNAome and measuring downstream interferon-stimulated gene (ISG) translation efficiencies. It showed that IFN-α dynamically remodels the mature tRNAome linked to amino acid metabolism and that disrupting tRNAome maturation or charging dampens antiviral efficacy. These results establish host tRNAome remodeling as a functional “decoding switch” that can bias translation toward antiviral or proviral programs.

Ou X, Lin X, Chen J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

The PLAGL1-KLF4-IRX5 axis promotes the osteogenesis of periosteal progenitors during mandible regeneration.

This study investigated how the imprinted transcription factor PLAGL1 regulates osteogenesis in adult periosteal stem/progenitor cells (PSPCs) during mandible regeneration, focusing on the PLAGL1–KLF4–IRX5 transcriptional axis. PLAGL1 was found to be critical for PSPC osteoblast differentiation, and its loss impaired mandibular bone regeneration by transcriptionally activating IRX5 synergistically with KLF4. These findings identify a specific TF network that could be targeted to improve craniofacial bone regenerative therapies.

Yao E, Liu Y, Xu J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Ribonuclease DIS3 delays aging and senescence by generating tRNA halves.

This study examined the role of tRNA halves (tRHs) in aging and longevity in metazoans, using a genetic screen in Caenorhabditis elegans to identify the ribonuclease DIS-3/DIS3 that generates tRHs. DIS3 was shown to catalyze production of specific tRHs (including 5’-tRH-Gln and 5’-tRH-Asp), and 5’-tRH-Gln was required for longevity from interventions such as dietary restriction by reducing translation via ribosomal protein binding and upregulating the SKN-1/NRF lifespan pathway. The work links a defined tRNA-processing enzyme and tRH species to conserved pro-longevity signaling, supporting tRH biology as a potential aging intervention target.

Ha SG, Lee H, Park J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Nitric oxide drives proteomic diversity through alternative splicing.

This study examined how nitric oxide (NO) regulates proteome diversity through alternative splicing by focusing on S-nitrosylation targets and the splicing regulator PTBP1. The key findings are that RNA-binding proteins (including spliceosomal factors) are enriched among S-nitrosylation targets, and that S-nitrosylation of PTBP1 shifts and contextually alters gene expression by changing PTBP1 RNA-binding domain conformation and interactions. Scientifically, it links NO redox signaling to widespread, mechanism-specific control of alternative splicing and transcriptome SNO-site enrichment.

Schindler JC, Seth P, Hausladen A et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

Ribo-Tweezer: Rapid removal of ribosomal proteins reveals additional layers of post-transcriptional gene regulation.

This study developed Ribo-Tweezer, a degron-based system tethered to mature ribosomes to rapidly and selectively deplete individual ribosomal proteins in situ, and applied it to mouse embryonic stem cells (mESC). The key finding is that using Ribo-Tweezer reveals a previously uncharacterized role for RACK1 in stem cell fate control via translational regulation of zinc-finger transcriptional networks. This is significant because it provides a new experimental tool to dissect non-housekeeping functions of ribosomal proteins in gene regulation.

Chen Y, Cheng CP, Cates K et al. · Molecular cell · (2026) · View on PubMed ↗

Reprogrammed apoptotic platelets drive rapid hemostasis through phosphatidylserine and prostaglandin E2 signaling in preclinical models.

This preclinical study developed a high phosphatidylserine (PS)-exposed procoagulant platelet (hPPL) derivative reprogrammed from isolated platelets using calcium ionophore A23187-induced apoptosis. In human and rat plasma and whole blood in vitro, hPPL promoted platelet activation and aggregation and showed superior hemostatic efficacy compared with clinical thrombin and commercial hemostatic products. The work suggests a PS/prostaglandin E2–linked platelet reprogramming approach as a potential rapid hemostasis therapy, including for patients at risk of uncontrolled bleeding.

Wang P, Du S, Wu S et al. · Science translational medicine · (2026) · View on PubMed ↗

Arl8b inactivates the Rab11a recycling pathway to promote LAMP1 sorting and lysosome biogenesis.

This cell biology study examined how the small GTPase Arl8b regulates lysosome biogenesis and sorting of newly synthesized LAMP1 by modulating the Rab11a recycling pathway. Using the RUSH assay, the authors found that Arl8b localizes to post-endocytic LAMP1 vesicles before fusion with acidic lysosomes, and Arl8b depletion caused Rab11a-dependent recycling of LAMP1 back to the plasma membrane, reducing lysosomal delivery. Mechanistically, Arl8b recruited the Rab11a GAP TBC1D9B to LAMP1-positive membranes, and TBC1D9B depletion similarly disrupted LAMP1 sorting, linking Arl8b–TBC1D9B control to lysosome biogenesis.

Chouhan P, Phogat Y, Walia K et al. · The Journal of cell biology · (2026) · View on PubMed ↗ · Free PDF ↗

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Plant Biology & Plant–Insect Interactions (brassinosteroid/FERONIA/thermotolerance, rice immunity, nutrient sensing)

Taking plant membrane temperatures.

This Science article investigated how plant plasma membrane nanoclusters encode and report membrane temperature to help plants distinguish beneficial warmth from damaging heat. It proposes that membrane nanocluster organization enables temperature discrimination at the plasma membrane level. Understanding this biophysical temperature-sensing mechanism could guide strategies to improve plant thermotolerance under climate warming.

Davis SJ, Ronald J · Science (New York, N.Y.) · (2026) · View on PubMed ↗

An appetite for protein.

This Science article studied how the Drosophila gut integrates nutrient-specific information to control protein appetite. It reports that gut nutrient sensing drives an appetite program tuned to protein availability. These findings advance mechanistic understanding of how peripheral nutrient signals shape feeding behavior, with implications for treating diet-related disorders.

Simpson SJ, Raubenheimer D · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Complex interplay of neuronal and hormonal gut-brain responses to essential amino acid deficit.

This Science study investigated how essential amino acid (EAA) deficit triggers coordinated neuronal and hormonal gut-brain responses in Drosophila. EAA deprivation increased CNMamide (CNMa) expression in gut enterocytes, activating enteric and brain neurons to promote EAA intake while CNMa suppressed DH44 sugar-sensing neurons to bias feeding away from carbohydrates and toward EAAs. These mechanisms identify a nutrient-specific gut-brain control circuit that could inform strategies to modulate appetite and metabolic regulation.

Kim B, Lee S, Bae H et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

FERONIA orchestrates plasma membrane nanoclusters for plant thermotolerance.

This Science article studied how the plant receptor kinase FERONIA (FER) organizes plasma membrane nanoclusters to drive thermotolerance in Arabidopsis. It shows that FER acts as a membrane-anchored thermal switch, activated by the RALF34 peptide under moderate heat, and nucleates sterol-dependent nanoclusters that stabilize liquid-ordered membrane phases and activate heat shock transcription factor signaling. The work links specific membrane biophysics and signaling organization to heat acclimation, offering targets for engineering heat-tolerant crops.

Wang K, Yan H, Guo X et al. · Science (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗

Plant Kelch phosphatases are Ser/Thr phosphatases involved in cell cycle regulation.

This plant molecular biology study investigated Kelch phosphatases and focused on how the brassinosteroid (BR) signaling component BSU1 functions as a Ser/Thr phosphatase-like regulator of cell growth. Structural analyses of the BSU1 phosphatase domain showed similarity to protein phosphatase 1 (PP1), and BSU1 was reported to dephosphorylate BR-pathway substrates (including phosphotyrosine sites in the BIN2 regulatory axis) consistent with its role in BR signaling. The work clarifies the biochemical nature of BSU1/plant Kelch phosphatases and advances understanding of how BR signaling is tuned to control plant cell cycle and growth.

Rico-Resendiz F, Pri-Tal O, Raia P et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

The effector NlOBP1b from the brown planthopper suppresses rice immunity by manipulating the OsCK2 complex.

This plant–insect interaction study characterized the brown planthopper (Nilaparvata lugens) salivary effector NlOBP1b and how it suppresses rice immunity by manipulating the OsCK2 complex. NlOBP1b-RNAi in brown planthopper reduced adaptability to host plants, and NlOBP1b was reported to interact with regulatory subunits of the OsCK2 complex (truncated in the abstract). The findings identify a specific effector–host kinase interaction that enables immune suppression, offering potential targets for engineering rice resistance against this major pest.

Wang C, Wei C, Qiu CL 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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Exercise, Rehabilitation & Human Performance (resistance exercise under mental fatigue, exercise immunology)

Mental Fatigue and Resistance Exercise: A Systematic Review and Meta-Analysis Including GRADE Qualification.

This systematic review and meta-analysis assessed how mental fatigue (MF) affects resistance exercise (RE) performance using randomized controlled trials in healthy human participants, applying GRADE qualification. It included studies with high-demand cognitive tasks (e.g., Stroop test) and low-demand/passive controls (e.g., watching documentaries) and synthesized 14 comparisons across 11 trials. The findings help clarify whether cognitive fatigue causally alters RE outcomes and support evidence-based guidance for training and performance under mental load.

Solon-Júnior LJF, Fortes LS, Vasconcelos G et al. · European journal of sport science · (2026) · View on PubMed ↗ · Free PDF ↗

The immunology of exercise: Mechanisms, mediators, and therapeutic opportunities.

This review synthesizes evidence from healthy individuals and disease contexts (notably cancer and autoimmunity) on how acute exercise bouts and chronic training modulate innate and adaptive immune cells and reprogram non-immune tissues (skeletal muscle, adipose tissue, vasculature, and gut microbiota). It highlights that exercise-induced signaling factors (“exerkines”)—including cytokines, metabolites, and catecholamines—reshape immune-cell mobilization, fate, and function to promote health and reduce disease risk. The work supports exercise as an immunotherapeutic strategy and identifies mechanistic targets for translating exercise biology into cancer and autoimmune interventions.

Phelps CM, Meisel M · Immunity · (2026) · View on PubMed ↗

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Generated automatically on May 23, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.