PubMed Trending Research Digest — June 30, 2026
A curated digest of 98 trending PubMed articles, automatically categorised and summarised across 15 research areas.
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PubMed Trending Research Digest — June 30, 2026
Automated digest · 98 articles · 15 research areas · June 30, 2026
Overview
Across this week’s set of papers, a dominant theme is precision targeting—either by identifying actionable biological vulnerabilities (e.g., receptor/ligand signaling mechanisms, protein degradation strategies, and lipid/sterol checkpoints) or by improving patient selection using biomarkers and computational frameworks. In oncology, multiple studies emphasize how resistance evolves under specific therapeutic pressures (ESR1-driven resistance to CDK4/6 inhibitors; asciminib resistance landscapes in CML) and how this knowledge can guide next-generation inhibitor design and treatment sequencing. Parallel efforts in precision oncology include AI/ML and multi-omics approaches (endometrial cancer, liver fibrosis risk, and systemic proteomic “age/atherosclerosis” signatures) that aim to translate high-dimensional biology into scalable clinical decision support.
A second major thread links immune modulation to disease modification across organ systems. In cancer, immune checkpoint function can be altered post-translationally (silibinin disrupting PD-L1 glycomaturation), while immune–microbiome interactions are highlighted as determinants of immunotherapy response (colorectal cancer ICI efficacy). In neuroinflammation and neurodegeneration, innate immune signaling (astrocyte innate pathways), specific immune cell programs (Csf1r+ myeloid cells in colitis-associated Parkinsonian pathology), and Treg-mediated control of acute CNS injury all underscore that immune circuits can be causal and therapeutically targetable.
Finally, several studies converge on metabolism, aging biology, and systemic physiology as modifiable drivers of outcomes. Work on senescent microenvironments, proteomic “age clocks,” and mitochondrial/ferroptosis-related interventions frames aging as a tractable biological state rather than a fixed risk. In cardiometabolic and cardiovascular domains, lipid-driven mechanisms (atherosclerosis, endothelial pyroptosis) and redox-active metabolite circuits (lactate/β-hydroxybutyrate) complement clinical efforts to standardize definitions and improve prediction of disease progression (heart failure consensus, fibrosis risk models, and cardiotoxicity multi-omics). Together, the digest reflects a broader shift toward mechanistic, biomarker-informed, and system-level interventions.
Cancer: Targeted therapy resistance & clonal evolution
Proteolytic EphA2 fragments cooperatively promote hepatocellular carcinoma progression.
This study investigated how proteolytic fragments of the EphA2 receptor tyrosine kinase—generated by MT1-MMP cleavage into an EphA2-C-terminal fragment (EphA2-CF) and an N-terminal fragment (EphA2-NF)—promote hepatocellular carcinoma (HCC) progression. The key finding was that EphA2-CF is present in HCC cells co-expressing EphA2 and MT1-MMP and that these cleavage fragments cooperatively drive malignant progression. Clinically, it identifies EphA2 cleavage-fragment biology as a potential mechanistic target to inhibit HCC progression.
Ikeda K, Asakura N, Sengoku S et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗
Beyond the JAK2 mutation: The inflammasome, clonal stability, and the thrombotic niche in myeloproliferative neoplasms.
This review synthesized evidence on why Philadelphia-negative myeloproliferative neoplasms (MPNs) have disproportionate thrombosis risk, focusing on clonal thrombo-inflammation driven by somatic mutations and innate immune activation. It highlights that JAK2V617F and other driver mutations reprogram myeloid cells toward hyperinflammatory states and links this to a continuum from clonal hematopoiesis of indeterminate potential (CHIP) to overt MPN. The mechanistic framework is clinically significant because it reframes MPN-associated thrombosis as a distinct biology that may require mutation- and inflammation-targeted strategies beyond conventional cardiovascular risk management.
Abdelgawwad El-Sehrawy AAM, Al-Khreisat MJ, Kibriyeva M et al. · Clinical and experimental medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Dual functional genomics reveals a broad and convergent landscape of asciminib resistance in BCR::ABL1.
This study used dual functional genomics to map a broad, convergent landscape of resistance mechanisms to asciminib in BCR::ABL1-driven chronic myelogenous leukemia (CML) models. Using a high-throughput adenosine base editing (ABE) screen to identify resistance hotspots and characterize epistatic effects, the key finding was that asciminib resistance can arise from multiple mutation patterns, including changes outside the kinase domain and from combinatorial interactions. Scientifically, this expands the actionable resistance map for asciminib and can inform next-generation inhibitor design and resistance-informed patient management.
Sokirniy I, Yang Z, Pritchard J · Genome medicine · (2026) · View on PubMed ↗ · Free PDF ↗
ESR1 mutations and CDK4/6 inhibitor choice shape clonal selection and adaptive cell states during acquired resistance.
This study examined how activating ESR1 mutations shape clonal selection and adaptive cell states during acquired resistance to CDK4/6 inhibitors in estrogen receptor-positive (ER+) metastatic breast cancer, using clonal dynamics analyses across treatment conditions with and without endocrine therapy. The authors report that ESR1 mutations are enriched after endocrine therapy plus a CDK4/6 inhibitor and that the specific choice of CDK4/6 inhibitor alters selective pressures, driving divergent resistance states and adaptive phenotypes. These findings support tailoring CDK4/6 inhibitor selection based on ESR1 mutation status to better anticipate and counter resistance evolution in ER+ breast cancer.
Guarducci C, Abravanel D, Russo D et al. · Genome medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer: Immunotherapy & immune checkpoint modulation
Engineered circular RNA compatible with complete nucleoside modification and rolling circle translation through a Cap-independent translation enhancer.
This work engineered a protein-encoding circular RNA (circRNA) that supports complete nucleoside modification and rolling circle translation (RCT) using a cap-independent translation enhancer (CITE) element from black beetle virus (BBV). The resulting “scarless” circRNA produced via in vitro transcription (IVT) enabled nucleoside-modified circRNA translation and showed superior anti-tumor inhibition compared with an m1ψ-mRNA vaccine in the reported experiments. The approach advances circRNA vaccine design by improving translational efficiency while maintaining enhanced stability and reduced immunogenic drawbacks.
Wang X, Pan Q, Yin J et al. · Nature biomedical engineering · (2026) · View on PubMed ↗
Atopic Dermatitis: New Targets and Emerging Systemic Therapies.
This narrative review studied emerging therapeutic targets and systemic treatments for atopic dermatitis (AD), focusing on how new biologics and oral small molecules address barrier and immune dysregulation. It reports that biologics and oral small molecules have improved outcomes but that complete durable clearance remains difficult, driving development of next-generation biologics targeting type 2 cytokines with advances in antibody bioengineering. The significance is that it maps the current pipeline of refined cytokine-targeted therapies and highlights ongoing unmet needs around long-term safety and treatment burden.
Avallone G, Beaziz J, Manzo Margiotta F et al. · American journal of clinical dermatology · (2026) · View on PubMed ↗
A bispecific-aptamer TSHR-CD80-1 treats thyroid eye disease by inhibiting CD8+ T cell-fibroblast interactions.
This study investigated thyroid eye disease (TED) by profiling peripheral blood leukocytes from TED patients and testing a bispecific-aptamer strategy using a TSHR-targeting nucleic acid aptamer (TSHR-21-42) to disrupt TSHR-mediated immune interactions. The key finding was that CD8+ T cell–orbital fibroblast interactions contribute to TED activity, and inhibiting this interaction reduced the pathogenic crosstalk. This is significant because it provides a mechanism-based therapeutic approach targeting immune–stromal interactions in an autoimmune disease.
Cao J, Chen Z, Feng L et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗
Effectiveness, Safety, and Drug Survival of Bimekizumab in Chronic Plaque Psoriasis over 2 Years: Real-World Experience from Northern Italy.
This retrospective, multicenter real-world study from three referral centers in Northern Italy assessed bimekizumab (a dual IL-17A/IL-17F inhibitor) in 126 adults with moderate-to-severe chronic plaque psoriasis over up to 2 years. The key finding was the real-world effectiveness and safety outcomes, including treatment persistence (“drug survival”) and achievement rates for PASI75/PASI90/PASI100. This is significant because it extends evidence for long-term performance of bimekizumab beyond clinical trials in routine practice.
Fratton Z, Bighetti S, Bettolini L et al. · Dermatology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Micellar curcumol reprograms tumor-associated macrophages and reverses PARP inhibitor resistance in recurrent ovarian cancer.
This study evaluated micelle-loaded curcumol (MC) for reprogramming tumor-associated macrophages (TAMs) and reversing PARP inhibitor resistance in recurrent ovarian cancer. In ID8-bearing mice with malignant ascites, it used single-cell RNA sequencing (scRNA-seq) to profile ascites immune transcriptomes and assessed effects on macrophages derived from patients with recurrent high-grade serous ovarian cancer receiving PARP inhibitor therapy (ROCAMs), focusing on sensitivity to niraparib. The results suggest MC as a macrophage-targeted strategy to overcome PARP inhibitor resistance in recurrent ovarian cancer.
Liu Q, Tang Q, Ye W et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
Silibinin is a natural molecular glue that inhibits PD-L1 glycomaturation.
This study investigated whether the natural flavonolignan silibinin (SBN) can inhibit interferon-γ (IFNγ)-driven PD-L1 glycomaturation and thereby enhance T-cell cytotoxicity in cancer models. SBN was found to impede PD-L1 glycomaturation, disrupting PD-L1’s functional maturation/trafficking to the cell surface and improving T-cell-mediated antitumor killing. These findings suggest silibinin could serve as a clinically feasible “molecular glue” strategy to weaken PD-L1 immune checkpoint function by targeting post-translational glycosylation rather than PD-L1 expression alone.
Teixidor-Vilà E, Encinar JA, Martin-Castillo B et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
Harnessing the gut microbiome for improved immune checkpoint inhibition in colorectal cancer immunotherapy: a narrative Review.
This narrative review examined how the gut microbiome can be leveraged to improve immune checkpoint inhibitor (ICI) efficacy in colorectal cancer immunotherapy. It summarizes evidence that microbiome composition and dysbiosis influence response and resistance to ICIs, with particular attention to why responses are stronger in mismatch repair-deficient (dMMR) tumors than in mismatch repair-proficient (pMMR) microsatellite-stable (MSS) disease. The review highlights microbiome-targeted strategies as a potential route to extend ICI benefit to broader colorectal cancer patient groups.
Abebaw D, Adugna A, Tegegne BA et al. · Clinical and experimental medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer: Antibody/biologic therapeutics & clinical trials
Extranodal natural killer/T-cell lymphoma: From fatal to curable.
This review studied the evolution of treatment strategies for extranodal natural killer/T-cell lymphoma (ENKTCL) in patients with NK- or T-cell–origin disease, particularly in EBV-associated, high-prevalence regions such as Asia and South America. It reports that ENKTCL outcomes have improved from historically fatal anthracycline-containing regimens to current combined-modality approaches that co-target genomic instability and metabolic vulnerability, with additional immune/metabolic targeting in some regimens. The clinical significance is that modern, mechanism-informed therapy paradigms have transformed ENKTCL from fatal to potentially curable disease.
Xiong J, Kwong YL, de Leval L et al. · CA: a cancer journal for clinicians · (2026) · View on PubMed ↗
Efficacy and safety of ofatumumab in participants with relapsing multiple sclerosis and breakthrough disease on oral fingolimod or fumarates: results from the ARTIOS study.
This phase 3b, open-label, single-arm ARTIOS study evaluated the efficacy and safety of ofatumumab in adults with relapsing multiple sclerosis (RMS) who had breakthrough disease while switching from oral fingolimod or fumarates. The key finding (relative to the study’s primary endpoint) is that ARTIOS assessed annualized relapse rate (ARR) and safety outcomes for this specific switching population after inadequate control on moderate-efficacy oral DMTs. Clinically, the results inform whether ofatumumab provides effective escalation therapy for RMS patients experiencing breakthrough disease on fingolimod or fumarates.
Bove R, Langdon D, Maciejowski M et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗
Comparison of Clinical Practice Guidelines for Chronic Hepatitis B: Natural History Classification and Treatment Initiation.
This review compared updated international and regional clinical practice guidelines for chronic hepatitis B (CHB)—specifically KASL-EALA, AASLD, EASL, and WHO—focusing on natural history classification, treatment initiation, and antiviral selection. Across guidelines, recommendations account for CHB’s heterogeneous, dynamic disease course, but differ in how patients are stratified and when antiviral therapy is started. These differences matter clinically because they can change eligibility for treatment and choice of agents, affecting long-term outcomes such as cirrhosis and hepatocellular carcinoma risk.
Kim GA, Choi WM, Choi GH et al. · Clinical and molecular hepatology · (2026) · View on PubMed ↗ · Free PDF ↗
Efficacy and safety of cabozantinib plus nivolumab in advanced non-clear cell renal cell carcinoma: a nationwide multicenter study.
This nationwide, multicenter retrospective cohort study evaluated cabozantinib plus nivolumab in 62 patients with advanced non-clear cell renal cell carcinoma (nccRCC) in the Republic of Korea, including multiple histologic subtypes such as papillary RCC and FH-deficient and TFE3-rearranged tumors. The key finding was the observed clinical activity and safety profile of the combination across treatment lines, with papillary RCC being the most common subtype (50.0%). These results are significant because they provide real-world evidence for a regimen that is not yet well defined for biologically heterogeneous nccRCC populations.
Kim CG, Kim J, Kim IH et al. · Oncoimmunology · (2026) · View on PubMed ↗ · Free PDF ↗
IMMPACT-MM: Insights into Multiple Myeloma Patient Outcomes following Early-Line Cilta-cel Treatment.
This real-world study evaluated outcomes, including minimal residual disease (MRD) negativity, in patients with relapsed/refractory multiple myeloma (RRMM) treated with cilta-cel (ciltacabtagene autoleucel) after 1–3 prior lines of therapy (LOT). The key finding was that early-line cilta-cel use was associated with clinically meaningful depth and durability of response, reflected by MRD negativity rates in this less heavily pretreated population. These data support MRD negativity as a functional-cure–relevant endpoint and help define the benefit-risk profile of cilta-cel when moved earlier in the treatment sequence.
Rajeeve S, Nagar SP, Ghosh S et al. · Oncology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Vibecotamab for measurable residual disease in acute myeloid leukemia and for myelodysplastic syndromes and chronic myelomonocytic leukemia after hypomethylating agent failure: a phase II study.
This phase II study evaluated vibecotamab, a CD123×CD3 bispecific antibody, for measurable residual disease (MRD) in acute myeloid leukemia (AML) and for MDS/CMML after hypomethylating agent failure. In patients with detectable AML-MRD and in those with MDS or chronic myelomonocytic leukemia post-hypomethylating agent failure, vibecotamab was assessed for clinical efficacy and safety as a targeted strategy to eliminate CD123-positive malignant cells via T-cell engagement. The trial is clinically significant because it tests an antibody-based approach for high-risk, treatment-limited settings where MRD persistence and post-hypomethylating agent relapse remain major unmet needs.
Short NJ, Bataller A, DiNardo CD et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer: Radioligand/radiotherapy & imaging-guided management
European guideline for imaging of primary paediatric and adult osteosarcoma and Ewing sarcoma: systematic review and joint statement by the FOSTER consortium, Euro Ewing Consortium, European Society of Paediatric Radiology, and the European Association of Nuclear Medicine.
This European guideline was developed by a multidisciplinary consortium using a systematic review of 2026 studies to standardize imaging for primary pediatric and adult osteosarcoma and Ewing sarcoma across diagnosis, staging, treatment response assessment, and post-therapy surveillance. The review found substantial heterogeneity in diagnostic criteria, chemotherapy regimens, and imaging protocols, with inconclusive evidence for the optimal modality to detect bone metastases and no consistent metabolic imaging indices or MRI parameters predicting response or survival. The guideline is significant because it aims to harmonize imaging practice to improve comparability in research and consistency in patient care.
Adriaansen LME, Merks JHM, van Dalen EC et al. · The Lancet. Oncology · (2026) · View on PubMed ↗
Dose escalation with intraoperative radiotherapy in newly diagnosed glioblastoma (INTRAGO-II): an open-label, multicentre, randomised, controlled, phase 3 trial.
This open-label, multicentre, randomized phase 3 trial (INTRAGO-II) studied whether adding intraoperative kilovoltage radiotherapy after resection improves outcomes in adults (18–80 years) with supratentorial newly diagnosed glioblastoma (KPS ≥60%). Patients were randomized to receive additional intraoperative radiotherapy versus standard of care, testing whether dose escalation reduces recurrence risk. If effective, this strategy could improve local control in glioblastoma by delivering targeted radiation at the time of maximal tumor debulking.
Giordano FA, Ganslandt O, Münter MW et al. · The Lancet. Oncology · (2026) · View on PubMed ↗
SBRT plus abiraterone acetate and ADT versus abiraterone acetate and ADT in oligometastatic castrate-resistant prostate cancer (ARTO): long-term, unplanned overall survival analysis of an open-label, randomised, phase 2 trial.
This long-term overall survival analysis of the open-label, randomized phase 2 ARTO trial evaluated whether stereotactic body radiotherapy (SBRT) as metastasis-directed therapy plus abiraterone acetate and androgen deprivation therapy (ADT) improves survival versus abiraterone acetate and ADT alone in oligometastatic castrate-resistant prostate cancer. The study focused on patients with prostate adenocarcinoma with metastatic castrate-resistant disease and no more than three metastatic sites. The clinical significance is that it tests whether early MDT provides durable overall survival benefit beyond initial response endpoints.
Francolini G, Di Cataldo V, Caini S et al. · The Lancet. Oncology · (2026) · View on PubMed ↗
Radioligand Therapy for Prostate Cancer - A Clinical Consultation Guide.
This clinical consultation guide reviewed evidence for PSMA-targeted radioligand therapy (RLT) in metastatic castration-resistant prostate cancer (mCRPC), focusing on [177Lu]Lu-PSMA-617 and landmark trials including VISION, TheraP, and PSMAfore. The key finding is that PSMA RLT improves survival and progression-free outcomes with defined safety and clinical roles, contingent on appropriate patient selection using PSMA PET imaging and disease burden assessment. This is significant because it translates trial-level efficacy into practical guidance for optimizing outcomes in mCRPC patients.
Hennes D, Al-Khanaty A, Monna M et al. · European urology focus · (2026) · View on PubMed ↗
Cancer: Molecular mechanisms & signaling targets
The mechanism for ligand activation of the Smoothened G protein-coupled receptor.
This study investigated the sequence of G protein and cholesterol (CHL) ligand binding to the Smoothened (SMO) G protein-coupled receptor in the Hedgehog (Hh) signaling pathway. The authors found results consistent with a G protein-first activation model in which CHL first binds the SMO cysteine-rich domain (CRD) while SMO remains inactive until G protein binding enables activation. These mechanistic insights clarify how SMO is activated and can inform targeted therapeutic strategies for Hh-driven cancers such as basal cell carcinoma.
Yu RD, Vo AP, Kim SK et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗
Functional Suppression of SCAP Triggers Endoplasmic Reticulum Stress-Dependent Ferroptosis by Impairing Cholesterol Metabolism in Gastric Cancer.
This study examined whether targeting the sterol-sensing domain (SSD) of SCAP (SREBP cleavage-activating protein) can trigger ferroptosis in gastric cancer (GC) by disrupting cholesterol metabolism. Using SSD structure-based high-throughput screening, the authors identified the natural compound Platycodin D (PD) as a SCAP inhibitor that sustains SREBP2 activation yet blocks cholesterol efflux by specifically disrupting SCAP’s sterol-sensing function, leading to endoplasmic reticulum stress-dependent ferroptosis. The findings are significant because they nominate SCAP-SSD as a druggable vulnerability and PD as a candidate small-molecule strategy for ferroptosis-based GC therapy.
Xu Q, Pan G, Zhang L et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗
Expanded Hepatic Progenitor Cells Featured with Aggregation of α-Synuclein Contribute to Pathologic Bile Duct Regeneration in Biliary Atresia.
This study investigated the cellular and molecular basis of ductular reaction (DR) and bile duct regeneration in biliary atresia (BA) using single-nucleus RNA sequencing and organoid models. It identified an expanded NCAM1+EpCAM+ hepatic progenitor cell (HPC) cluster as predominant in DR, showed that α-synuclein is the signature gene of this cluster and is upregulated in human and mouse BA tissues and patient serum, and demonstrated that α-synuclein–associated organoids have impaired biliary differentiation. The significance is that α-synuclein–marked HPCs contribute to pathological regeneration in BA, suggesting a potential target to improve biliary repair.
Xie H, Zhu M, Zhu Z et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Phase 3 Trial of Oral Infigratinib in Children with Achondroplasia.
This phase 3 multicenter, double-blind, placebo-controlled trial studied oral infigratinib (FGFR1–3 tyrosine kinase inhibitor) in children with achondroplasia aged 3 to 17 years. The key finding was not fully visible in the truncated abstract text, but the primary endpoint was the change from baseline in annualized height velocity at week 52 versus placebo. Clinically, positive results would support an oral, pathway-targeted therapy for achondroplasia driven by FGFR3 pathogenic variants.
Savarirayan R, Hoover-Fong J, Irving M et al. · The New England journal of medicine · (2026) · View on PubMed ↗
The effect of TIPS on the development of hepatocellular carcinoma in patients with cirrhosis: a meta-analysis.
This meta-analysis assessed whether transjugular intrahepatic portosystemic shunt (TIPS) is associated with the development of hepatocellular carcinoma (HCC) in patients with cirrhosis. The key finding was the pooled estimate of the association between TIPS and subsequent HCC risk across included studies (with the study designed to resolve prior controversy). This is clinically significant because it informs risk–benefit decisions when using TIPS for ascites or gastrointestinal bleeding in cirrhosis.
Xu X, Jiang M, Fu Y et al. · BMC gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗
Gαo/z-biased coupling profile of the dopamine D3 receptor.
This study characterized the G protein coupling profile of the dopamine D3 receptor (D3R) and compared it with D2-like dopamine receptors in the context of GPCR signaling. The key finding was D3R’s striking inability to engage Gαi proteins effectively, defining a distinct Gαo/z-biased coupling behavior. This mechanistic insight can guide the design of safer dopamine D3R-targeted therapeutics with fewer on-target side effects.
Zanetti L, Franchini L, Saha S et al. · Communications biology · (2026) · View on PubMed ↗ · Free PDF ↗
Bufalin suppresses breast cancer bone metastasis through targeting SEC13-mediated osteoclastogenesis.
This study tested whether bufalin suppresses breast cancer bone metastasis by targeting SEC13-mediated osteoclastogenesis. Using in vivo murine models of breast cancer bone metastasis and in vitro/in vivo osteoclast assays, it showed that bufalin inhibited osteoclast differentiation and osteolytic bone destruction, implicating SEC13 as a key mechanistic node. These findings position SEC13-dependent osteoclastogenesis as a therapeutic target and bufalin as a candidate anti-metastatic agent for osteolytic breast cancer progression.
Li Z, Li X, Yu X et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
The role of the WD40-repeat protein family in cancer.
This review analyzed the WD40-repeat (WDR) protein family, focusing on how WD40 β-propeller structural logic enables scaffold functions across transcription/epigenetic regulation, ubiquitin-dependent proteostasis, RNA metabolism, and cell-cycle control in cancer. It synthesizes evidence linking WDR structural features to context-dependent oncogenic mechanisms and highlights gaps in connecting these mechanisms to actionable biomarkers and therapeutic strategies. By framing WDR proteins as structurally grounded, functionally modular cancer drivers, the article supports more rational biomarker discovery and drug targeting approaches.
Li J, Zhou H, Luo Q et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer: Biomarkers & multi-omics/AI for precision oncology
Peripheral blood immune profiling reveals key signatures in newly diagnosed NK/T cell lymphoma patients.
This study profiled peripheral blood immune signatures in newly diagnosed natural killer/T-cell lymphoma (NKTCL) patients using single-cell RNA sequencing of PBMCs, with validation by flow cytometry and PrimeFlow. It identified a distinct proliferative NK/T (Proli-NK/T) cell subset associated with NKTCL, distinguishing patients from healthy donors. The findings are significant because they suggest a systemic immune biomarker signature at diagnosis that could improve risk stratification and guide therapeutic targeting in EBV-associated NKTCL.
Li D, Zou H, Wang M et al. · Theranostics · (2026) · View on PubMed ↗ · Free PDF ↗
Dual phosphoregulatory mechanisms of condensin I revealed by biochemical reconstitution.
This biochemical reconstitution study investigated how mitotic chromatin transformations are controlled by dual phosphoregulatory mechanisms of condensin I using a minimal set of recombinant proteins. It found that cyclin B–Cdk1 phosphorylates terminal intrinsically disordered regions (tIDRs) of non-SMC subunits to release condensin I from self-suppression, and that Cdk1 phosphorylation of a conserved CAP-H (kleisin) residue is essential for proper condensin I function. Scientifically, it clarifies how Cdk1-driven phosphorylation coordinates condensin assembly/disassembly during mitosis, advancing mechanistic models of chromosome segregation.
Shintomi K, Tane S, Masahara-Negishi Y et al. · PNAS nexus · (2026) · View on PubMed ↗ · Free PDF ↗
Proliferative ecotype determines lethal prognosis and therapeutic benefit in urothelial carcinoma.
This multi-cohort study of 1431 urothelial carcinoma (UC) patients investigated whether tumor proliferation, operationalized as a “proliferative ecotype,” improves molecular classification and predicts prognosis and therapeutic benefit beyond Ki-67 alone. Using an integrated multi-omics framework with experimental validation, it assessed how proliferative status shapes tumor microenvironment features and therapeutic vulnerabilities, with the specific results not fully shown in the truncated abstract. Clinically, incorporating proliferative ecotype concepts could refine risk stratification and identify patients more likely to benefit from targeted therapies in UC.
Sun J, Jin K, Ding Y et al. · Cancer · (2026) · View on PubMed ↗
Engineered Heart Tissues Facilitate Noncoding Variant Studies in Cardiomyopathy.
This study investigated how engineered heart tissues (EHTs) built from human induced pluripotent stem cell-derived cardiomyocytes and primary cardiac fibroblasts can be used to test noncoding variants implicated in cardiomyopathy. The key finding is that combining single-cell gene expression with chromatin accessibility to generate genome-wide regulatory maps enables functional prioritization of noncoding regulatory elements in a human genome context. The scientific significance is that this EHT-based regulatory mapping approach provides a scalable experimental platform to move beyond GWAS loci in poorly conserved noncoding regions toward mechanistic cardiomyopathy variant interpretation.
Weber ZT, Monroe TO, Holgren C et al. · Circulation research · (2026) · View on PubMed ↗
Integrating artificial intelligence and multi-omics data for precision oncology in endometrial cancer: a narrative review.
This narrative review evaluated how integrating artificial intelligence/machine learning with multi-omics data can improve precision oncology for endometrial cancer, focusing on clinically challenging no specific molecular profile (NSMP) and mismatch repair-deficient (MMRd) subgroups. The key finding is that AI/ML can better capture endometrial cancer biological heterogeneity beyond conventional histopathology, imaging, and single-layer molecular profiling. This supports more accurate diagnostic, prognostic, and therapeutic decision-making frameworks for endometrial cancer patients.
Mondal O, Khatun M, Lawarde A et al. · Functional & integrative genomics · (2026) · View on PubMed ↗ · Free PDF ↗
Explainable machine learning models predict liver fibrosis risk and outcome in the general population: Development and multi-cohort external validation.
This study developed and externally validated explainable machine learning models to predict liver fibrosis risk and outcomes in the general population using readily available demographic, anthropometric, and clinical variables. In 9,424 European UK Biobank participants (with 1,678 classified as high risk by FIB-4 ≥1.45 or NFS ≥ −1.455), XGBoost was among the best-performing interpretable models and was further validated in a separate 2017–2023 National Health dataset. The approach supports scalable, population-level pre-screening for significant liver fibrosis using transparent ML rather than relying solely on invasive or specialist-dependent testing.
Zhu G, Yi Q, Xu R et al. · Computer methods and programs in biomedicine · (2026) · View on PubMed ↗
Mass Spectrometry Insights Into Post-Translational Modifications in Extracellular Vesicles.
This review article examined how mass spectrometry can characterize post-translational modifications (PTMs) in extracellular vesicles (EVs), focusing on EV proteomics and the shift toward understanding PTM-defined cargo. The key finding is that advanced mass spectrometry workflows enable detailed mapping of EV PTMs, which is increasingly important for interpreting EV function and biomarker potential. Scientifically, this supports PTM-aware EV analysis as a route to better biomarker discovery, therapeutic target identification, and EV-based drug delivery design.
Virág D, Karvaly KM, Molnár A et al. · Mass spectrometry reviews · (2026) · View on PubMed ↗
Navigating AI and machine learning in cancer research: an end-to-end translational framework.
This translational review studied how to operationalize artificial intelligence (AI) and machine learning (ML) across the cancer research pipeline, covering preclinical studies, clinical decision support, and real-world deployment. It proposes an end-to-end computational framework intended to address limitations of current methods for analyzing high-dimensional, multi-level cancer data. The framework is significant because it provides a practical roadmap for converting AI/ML models into clinically usable tools while managing translational and implementation challenges.
Saha S, Ali MS, Tengli AK et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer: Protein degradation & epigenetic/druggable vulnerabilities
Aryl Aldehyde-Anchored Small Molecules Recruit FBXO22 for Targeted Degradation of NSD2.
This medicinal chemistry study reported an aldehyde-anchored PROTAC that covalently recruits the E3 ligase FBXO22 to induce targeted degradation of the histone methyltransferase NSD2 (and CDK12). The key finding was that the lead degrader T9 selectively and effectively induces NSD2 degradation across multiple cancer cell lines, with degradation dependent on the steric/electronic properties of the aldehyde warhead. The work is significant because it expands the limited repertoire of E3 ligase recruiters for targeted protein degradation and provides a strategy for pharmacologically modulating NSD2-driven cancer biology.
Tang H, Liao Y, Yeh TY et al. · Journal of medicinal chemistry · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Neurodegeneration & neuroinflammation (incl. EV-mediated spread)
Innate immune signaling and functions in astrocytes.
This Review synthesized current evidence on innate immune signaling pathways in astrocytes, emphasizing pattern recognition via Toll-like receptors, nucleic acid sensors, and inflammasome activation. It highlights how downstream interferon, NF-κB, and STAT3 signaling drives astrocyte reactivity and functions such as cytokine secretion, antiviral responses, and phagocytosis. The article is significant because it frames astrocyte innate immunity as both protective for CNS health and a contributor to neuroinflammatory disease when dysregulated.
Guo AX, Fisher TM, Comandante-Lou N et al. · Nature immunology · (2026) · View on PubMed ↗
Arc mediates intercellular tau transmission via extracellular vesicles.
This study investigated how the neuronal gene Arc mediates intercellular tau transmission via extracellular vesicles (EVs). Arc knockout reduced tau content and tau seeding potential in brain EVs from rTg4510 mutant tau mice, and Arc and tau were co-packaged in mouse and human brain-derived EVs with EV-tau levels correlating with Arc levels in human Alzheimer’s disease brains. These findings identify Arc as a mechanistic driver of EV-mediated tau spread, offering a potential target to slow neurodegenerative propagation.
Tyagi M, de Hoog E, Grega M et al. · Cell · (2026) · View on PubMed ↗
Prior Traumatic Brain Injury and Alzheimer Disease Blood Biomarkers.
This cross-sectional diagnostic test study evaluated the accuracy of FDA-approved plasma Alzheimer disease (AD) blood biomarkers—specifically the p-tau217/Aβ42 ratio and related measures—in US veterans with and without a history of traumatic brain injury (TBI). The key finding (as framed by the study objective) is that the performance of these emerging biomarkers for detecting brain amyloid positivity was assessed specifically in the TBI-exposed veteran population, where TBI is known to alter AD blood biomarker levels. Scientifically, the work addresses whether p-tau217/Aβ42 and p-tau217/Aβ42/40 metrics remain reliable for amyloid detection in a high-risk clinical subgroup with prior brain injury.
Rosen-Lang Y, Vrillon A, Pasternak S et al. · JAMA neurology · (2026) · View on PubMed ↗
Immune Cells as Mediators Between Gut Microbiota and Multiple Sclerosis: Insights From Mendelian Randomization.
This Mendelian randomization study investigated causal relationships between gut microbiota taxa, immune traits, and multiple sclerosis (MS) using genetic data from 18,340 participants for microbiota, 3,757 for immune traits, and 47,429 MS cases with 68,374 controls. The key finding is that six microbial taxa (as suggested by the truncated results) and associated immune features showed evidence consistent with causal involvement in MS risk. The significance is that it provides genetically supported leads for immune-mediated gut–brain mechanisms that could guide microbiome- or immune-targeted MS prevention or therapy.
Ning P, Mu X, Zhang X et al. · Immunity, inflammation and disease · (2026) · View on PubMed ↗ · Free PDF ↗
Novel treatments for Parkinson’s disease.
This narrative review summarized novel and emerging disease-modifying and symptomatic treatments for Parkinson’s disease (PD), including approaches such as continuous dopaminergic stimulation, adaptive deep brain stimulation, transcranial temporal interference stimulation, and anti-α-synuclein immunotherapies/oral therapies. The key finding is that multiple strategies targeting neuroprotection and α-synuclein pathology are advancing beyond symptomatic-only care, aiming to slow progression. This is clinically significant because it highlights therapeutic directions that could improve long-term outcomes beyond the waning efficacy of currently approved symptomatic drugs.
Yin Y, Gao J, Zhang K et al. · Chinese medical journal · (2026) · View on PubMed ↗ · Free PDF ↗
Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.
This review synthesized mechanistic and therapeutic evidence on regulatory T cells (Tregs) as modulators of acute brain injury across conditions including acute ischemic stroke, traumatic brain injury, intracerebral hemorrhage, and subarachnoid hemorrhage. The key finding is that Tregs counteract effector T cell–driven neuroinflammation by promoting immunosuppression and tissue repair, thereby supporting blood–brain barrier integrity and resolution of inflammation. This is significant because it frames Treg-based strategies as promising approaches for neuroprotection and improved outcomes after acute CNS injury.
Ansari J, Sasannia S, Matsyuk M et al. · Molecular neurobiology · (2026) · View on PubMed ↗ · Free PDF ↗
GDAP1 orchestrates redox signaling at membrane contact sites to preserve axonal integrity in Charcot-Marie-tooth disease.
This study examined how the Charcot-Marie-Tooth disease gene GDAP1 preserves axonal integrity by orchestrating redox signaling at membrane contact sites (MCSs) in neurons. Using a multi-tier approach including high-resolution/live-cell imaging, pH-sensitive probes, MCS analysis, lipid studies, transcriptomics, and nerve ultrastructural assessment, it found that GDAP1 regulates redox-dependent inter-organelle communication at MCSs. The findings are significant because they connect GDAP1’s redox-sensor function to the cellular mechanisms underlying axonal degeneration in CMT.
Cantarero L, Roldán M, Rodríguez-Sanz M et al. · Neurobiology of disease · (2026) · View on PubMed ↗ · Free PDF ↗
Multi-strategy investigation identifies amentoflavone as a novel D3R antagonist for Parkinson’s disease treatment.
This study used a multidisciplinary strategy to identify the direct protein target of the biflavonoid amentoflavone (AMF) and characterize its mechanism as a D3R antagonist for Parkinson’s disease treatment. It focused on AMF’s anti-parkinsonian effects and proposed dopamine D3 receptor (D3R) antagonism as the mechanistic basis, aiming to connect target engagement with neuroprotective outcomes in PD models. The work provides a mechanistic rationale for AMF as a potential disease-modifying or symptom-improving natural-product lead targeting D3R.
Chen H, Zhang Y, Peng XJ et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
Current perspectives on the pathogenesis of multiple sclerosis: A minireview.
This minireview summarized current understanding of multiple sclerosis (MS) pathogenesis, integrating genetic, immunologic, and environmental contributors and highlighting emerging mechanisms. It emphasizes roles for Epstein–Barr virus immune responses, blood–brain barrier disruption, microbiome–gut–brain axis alterations, oxidative damage, and mitochondrial dysfunction in driving heterogeneous MS pathology. Scientifically, the synthesis supports more targeted research directions and may guide future biomarker and therapeutic development across MS subtypes.
Radikova Z, Tibensky M, Mosna L et al. · Endocrine regulations · (2026) · View on PubMed ↗ · Free PDF ↗
Long-term functional synaptic integration of genome-edited retinal organoids in a primate model of macular degeneration.
This primate translational study tested whether genome-edited ISL1-/- human retinal organoids (lacking ON-bipolar cells) can integrate functionally after transplantation into an acute laser-induced macular photoreceptor ablation model in nonhuman primates. Using immunohistochemistry, ultrastructural imaging, and focal macular electroretinography (FMERG), the study found that host rod and cone bipolar cells extended dendrites to grafted photoreceptors, formed synaptic contacts, and showed evidence of functional synaptic integration over the long term. This is significant because it demonstrates durable, circuit-level rewiring potential for gene-edited retinal organoid therapies in a primate model relevant to macular degeneration.
Ozaki A, Kawai A, Akiba R et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Lysophagy protects against ANXA11 amyloid fibril toxicity and propagation in FTLD.
This translational neurodegeneration study tested whether lysophagy protects neurons against Annexin A11 (ANXA11) amyloid fibril toxicity and propagation in frontotemporal lobar degeneration (FTLD). Using pre-formed fibrils (PFFs) of wild-type and FTLD/ALS-linked D40G mutant ANXA11, along with human iPSC-derived neurons and 3D cerebral organoid models, the key finding was that lysophagy/lysosomal integrity limits ANXA11 proteinopathy-related toxicity and intercellular spread. This is clinically significant because it identifies lysophagy as a potential therapeutic checkpoint for ANXA11-driven neurodegenerative disease progression.
Zheng H, Luo H, Lu Y et al. · Translational neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗
Csf1r-mediated depletion of myeloid cells prevents dopaminergic neuron loss during chronic colitis.
This study examined whether Csf1r-mediated depletion of myeloid cells prevents dopaminergic neuron loss during chronic colitis in adult mice, linking gut inflammation to neurodegeneration. Using confocal microscopy and integrated multi-omics with single-cell mapping of the midbrain immune response, the authors show that depleting Csf1r-dependent myeloid populations reduces substantia nigra pars compacta dopaminergic neuron loss and synuclein pathology. The findings support a causal role for specific brain immune cell programs in colitis-associated Parkinsonian pathology and identify Csf1r+ myeloid cells as a potential therapeutic target.
Kutscherauer RK, Andert M, Stolzer I et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗
Neuroscience: Pain, circuits & neuroplasticity
Prenatal Acetaminophen (Paracetamol) Use and the Risk of Autism and/or Attention-Deficit/Hyperactivity Disorder Among Sibling-Matched Cohorts.
This population-based sibling-matched cohort study examined whether prenatal acetaminophen (paracetamol) exposure is associated with offspring risk of autism spectrum disorder (ASD) and/or attention-deficit/hyperactivity disorder (ADHD). By using sibling matching to control for unmeasured familial confounding, it aimed to estimate the association of prenatal paracetamol with neurodevelopmental outcomes in offspring. The clinical significance is that it directly tests a widely used prenatal medication’s potential neurodevelopmental risk while strengthening causal inference compared with conventional observational designs.
Luo S, Gong Q, Ai Y et al. · JAMA internal medicine · (2026) · View on PubMed ↗
Migraine and auditory dysfunction: beyond comorbidity.
This review studied migraine as a multisensory sensitization disorder and focused on auditory dysfunction phenotypes such as sensorineural hearing loss, tinnitus, and hyperacusis. It reports that a substantial fraction of migraine patients experience comorbid auditory symptoms and that many show auditory electrophysiological abnormalities, while noting that mechanistic understanding and standardized audiological assessment and treatment evidence remain incomplete. The scientific significance is that it frames auditory manifestations as clinically important features of migraine that may require targeted evaluation beyond comorbidity.
Xu W, Zhai N, Chen J et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗
A descending posterior insular pathway drives sensory hypersensitivity in neuropathic pain.
This study investigated how specific insular cortex (IC) circuits regulate neuropathic pain in a chronic constriction injury (CCI) mouse model, focusing on posterior IC glutamatergic (pICGlu) and anterior IC glutamatergic (aICGlu) neurons. The key finding is that pICGlu neurons are selectively and contralaterally activated by CCI and bidirectionally regulate pain sensitivity, while aICGlu neurons preferentially drive CCI-induced anxiety-like behaviors, with circuit mapping implicating projections to rostral ventromedial medulla (RVM) GABAergic neurons. The scientific significance is that it identifies separable IC subcircuits as mechanistic targets for modulating sensory hypersensitivity versus affective components of neuropathic pain.
Ding H, Zou L, Ma L et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗
Central sensitization and hormonal therapy failure for endometriosis-related pain symptoms: a prospective study.
This prospective single-center observational cohort study evaluated 114 endometriosis patients for associations between central sensitization (measured by the Central Sensitization Inventory, CSI) and hormonal therapy failure (HTF). The key finding (as investigated by the study design) is whether higher CSI/central sensitization scores predict failure of hormonal therapy for endometriosis-related pain symptoms. Clinically, establishing this link could enable earlier stratification of patients who may need alternative or intensified pain and disease management strategies.
Raimondo D, Bertoldo L, Aguzzi A et al. · Journal of minimally invasive gynecology · (2026) · View on PubMed ↗
Psilocybin reduces fear memory and restores neuroplasticity in the hippocampus and medial prefrontal cortex.
This preclinical mouse study tested whether psilocybin reduces auditory-cued fear memory and restores neuroplasticity in the hippocampus and medial prefrontal cortex (mPFC) in a PTSD-like model. The key finding was that psilocybin treatment (2.5 mg/kg, intraperitoneal) improved fear-memory outcomes and promoted neuroplasticity-related changes in these brain regions. This is significant because it supports a mechanistic rationale for psilocybin as a potential therapeutic approach for PTSD and comorbid depressive symptoms via hippocampal–mPFC plasticity modulation.
Du Y, Zhao X, Yao Y et al. · Journal of psychopharmacology (Oxford, England) · (2026) · View on PubMed ↗
Effect of “Tongdu Yupi Tiaoshen” electroacupuncture on behavioral performance and hippocampal structure and function in chronic fatigue syndrome rats.
This animal study investigated whether electroacupuncture using “Tongdu Yupi Tiaoshen” improves behavioral performance and hippocampal structure/function in chronic fatigue syndrome (CFS) rats. In a rat model induced by 21 days of chronic multi-factor compound stress, electroacupuncture for 14 days produced better behavioral outcomes and normalized hippocampal structural and functional measures compared with modeled controls. The findings are significant as they suggest a neurobiological mechanism for electroacupuncture in CFS and provide preclinical support for further mechanistic and translational studies.
Yuanyuan QU, Chuwen F, Weibo S et al. · Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · (2026) · View on PubMed ↗ · Free PDF ↗
Infectious disease: Antimicrobial resistance & surveillance
Enhanced invasiveness promotes the dominance of a widely-distributed carbapenem-resistant virulence-plasmid-carrying Klebsiella pneumoniae sublineage.
This surveillance and genomic study analyzed 1,513 clinical carbapenem-resistant Klebsiella pneumoniae (CRKP) isolates over 10 years using whole-genome sequencing, alongside fine-scale analysis of 60,724 public K. pneumoniae genomes, to characterize a dominant ST11-KL64 sublineage. The authors found that this widely disseminated sublineage carried virulence-associated plasmids (“hypervirulence” factors) and showed enhanced invasiveness, with increased recovery during seasonal influenza peaks. Clinically, the results identify a high-risk CRKP lineage with epidemic-season associations, informing infection control and antimicrobial resistance/virulence monitoring.
Yang Y, Qin J, Feng Y et al. · Nature communications · (2026) · View on PubMed ↗
Clarithromycin Resistance Patterns of Helicobacter pylori across Different Gastric Diseases in Uzbekistan.
This retrospective study assessed clarithromycin resistance patterns of Helicobacter pylori across different gastric diseases in Uzbekistan, analyzing 279 patients with chronic non-atrophic gastritis, chronic atrophic gastritis, gastric ulcer, MALT lymphoma, or gastric cancer. Clarithromycin resistance was characterized using 23S rRNA mutations (A2142G, A2142C, A2143G) and/or eradication treatment failure, revealing disease- and genotype-associated resistance patterns. Clinically, these data can inform local selection of eradication regimens and molecular testing strategies to improve H. pylori treatment success in Uzbekistan.
Yusupbekov A, Shinozuka T, Ismailova J et al. · Journal of gastrointestinal and liver diseases : JGLD · (2026) · View on PubMed ↗ · Free PDF ↗
Calcineurin-Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in Candida Glabrata.
This study investigated how calcineurin-dependent stress adaptation enables caspofungin heteroresistance and stable resistance in Candida glabrata. In a multicenter collection of 156 isolates, heteroresistance was prevalent and caspofungin-specific, and transcriptomics implicated the calcineurin pathway; importantly, the resistant phenotype was abolished by calcineurin pathway inhibition and by deleting Δcnb1 and Δcrz1. These findings identify the calcineurin–Crz1 axis as a mechanistic driver of antifungal resistance evolution, suggesting potential targets to prevent or treat caspofungin resistance.
Su Y, Li Y, Xiao M et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Comparative efficacy and safety of oral ivermectin, topical permethrin, and combination in the treatment of patients with classic scabies: systematic review and network meta-analysis.
This systematic review and network meta-analysis compared oral ivermectin, topical permethrin, and their combination for classic scabies, focusing on comparative efficacy and safety in patients. The key finding was a relative ranking of these regimens by treatment outcomes and adverse events across randomized controlled trials, clarifying where oral ivermectin (alone or with permethrin) may outperform or match topical therapy. This is significant for clinicians and policymakers because it provides evidence-based guidance for selecting second-line versus combination strategies when permethrin is inadequate or adherence is a concern.
Genuino RF, Batac MCFR, Yacapin CPRC et al. · BMC pharmacology & toxicology · (2026) · View on PubMed ↗ · Free PDF ↗
Infectious disease: Antiviral/zoonotic surveillance
Genomic and structural evidence of SARS-CoV-2 and MERS-CoV in migratory birds.
This study used genomic and structural analyses to test whether SARS-CoV-2 and MERS-CoV are present in migratory birds, reporting three almost full-length SARS-CoV-2 variant-of-concern genomes from tundra swans. The identified SARS-CoV-2 sequences (IMCAS_M1, IMCAS_M2, IMCAS_M3) contained spike receptor-binding domain mutations matching Beta (K417N, E484K, N501Y) and Gamma (K417T, E484K, and related) variant patterns. The scientific significance is that it provides evidence of SARS-CoV-2 circulation in avian hosts and supports continued surveillance of wildlife reservoirs for potential viral evolution and spillover risk.
Cao J, Liu S, Su C et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗
Cardiovascular disease: Heart failure definitions, remodeling & cardiotoxicity
ZER1 Restrains Pressure Overload-Induced Cardiac Remodeling by Targeting DVL2 for Gly/N-Degron-Dependent Degradation.
This study investigated how Zyg-11-related regulator 1 (ZER1) regulates proteostasis to restrain pressure overload-induced cardiac remodeling in human failing hearts and mouse transverse aortic constriction (TAC) models. It found that ZER1 loss—globally or specifically in cardiomyocytes—worsens TAC-induced hypertrophy, fibrosis, and systolic dysfunction, and that ZER1 promotes Gly/N-degron-dependent degradation by directly binding disheveled segment polarity protein 2 (DVL2) via an N-terminus-dependent interaction. The clinical significance is that ZER1–DVL2 proteostatic control may represent a therapeutic target to prevent maladaptive remodeling and heart failure progression.
Jiang M, Lin Z, Chen L et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗
HIgh versus STAndard blood Pressure target in hypertensive high-risk patients undergoing elective major abdominal surgery: the HISTAP multicenter randomized clinical trial.
The HISTAP multicenter randomized clinical trial studied intraoperative mean arterial pressure (MAP) targets in elderly, high-risk hypertensive patients undergoing elective major abdominal surgery, comparing MAP ≥80 mmHg versus MAP ≥65 mmHg. The key finding was not fully visible in the provided abstract text, but the trial design targeted whether the higher MAP strategy reduces postoperative organ dysfunction and 30-day mortality in this population. If confirmed, the results would directly inform intraoperative hemodynamic targets for high-risk hypertensive surgical patients.
Cecconi M, Cortegiani A, Noto A et al. · Intensive care medicine · (2026) · View on PubMed ↗
AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026).
This AHA/ACC/ESC/WHF Expert Consensus Document (Second Universal Definition of Heart Failure, 2026) studied how to standardize definitions of heart failure (HF) and its antecedent stages to reduce ambiguity in research and surveillance. It found that prior stage B (“pre-HF”) concepts and subsequent advances have improved prevention, diagnosis, and management frameworks while highlighting global disparities and the importance of patient voice. Scientifically and clinically, the consensus provides a unified HF definition to improve comparability across studies and to guide prevention and care strategies worldwide.
Walsh MN, Kober L, Sliwa K et al. · Journal of the American College of Cardiology · (2026) · View on PubMed ↗
Catheter ablation of atrial fibrillation in transthyretin and light-chain cardiac amyloidosis: results from the multicentre AMYL-AF study.
The multicentre AMYL-AF registry studied outcomes of atrial fibrillation (AF) catheter ablation in patients with cardiac amyloidosis, specifically transthyretin (ATTR) and light-chain (AL) disease. It evaluated AF atrial arrhythmia recurrence and a composite of all-cause mortality and heart failure hospitalization (HFH), with results not fully shown in the truncated abstract. The study is significant because it addresses the evidence gap on ablation efficacy and safety in amyloid cardiomyopathy, where AF is common and prognosis is poor.
Faccenda D, Bergonti M, De Potter T et al. · Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · (2026) · View on PubMed ↗
AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026).
This 2026 AHA/ACC/ESC/WHF expert consensus document studied how to standardize the universal definition of heart failure (HF) across populations, building on the 2021 framework that defined stage B (pre-HF). It key findings that the updated consensus clarifies definitions for HF and its antecedent stages to reduce subjectivity and improve global surveillance, prevention, diagnosis, and management while incorporating patient voice. The clinical significance is that harmonized HF staging and diagnostic criteria should improve comparability of research and enable more consistent identification of at-risk individuals worldwide.
Walsh MN, Kober L, Sliwa K et al. · Circulation · (2026) · View on PubMed ↗
AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026).
This 2026 AHA/ACC/ESC/WHF expert consensus document studied standardizing the universal definition of heart failure (HF) and its antecedent stages across diverse global settings. The key finding is that it refines the 2021 stage B (pre-HF) concept to better support prevention and improve HF diagnosis and management while addressing disparities and the importance of patient-reported perspectives. Scientifically, the significance is that clearer, less ambiguous HF definitions should strengthen research design, global monitoring, and prevention programs.
Walsh MN, Kober L, Sliwa K et al. · European heart journal · (2026) · View on PubMed ↗
Decreasing Microtubule Detyrosination Improves Cardiac Mechanics and Sodium Channel Function in Arrhythmogenic Cardiomyopathy.
This study examined whether decreasing microtubule detyrosination affects cardiac mechanics and cardiac sodium channel distribution/function in mouse and human models of arrhythmogenic cardiomyopathy. The key finding is that reduced microtubule detyrosination improves membrane mechanical properties and restores aspects of sodium channel function and localization, linking microtubule post-translational state to arrhythmia-relevant electrophysiology. The clinical/scientific significance is that microtubule detyrosination emerges as a potential therapeutic target to mitigate sodium-channel dysfunction in arrhythmogenic cardiomyopathy.
Nasilli G, Lin X, Swiatlowska P et al. · Circulation. Arrhythmia and electrophysiology · (2026) · View on PubMed ↗ · Free PDF ↗
Cardiac remodelling and dysfunction in cancer patients receiving cardiotoxic therapies: proteomic and metabolomic profiling.
This longitudinal prospective cohort study investigated how circulating proteomic and metabolomic profiles relate to cardiac remodeling and dysfunction in breast cancer patients receiving cardiotoxic therapies, specifically anthracyclines and/or trastuzumab. The key finding is that repeated-measures proteomics (Olink Explore 3072) and rapid liquid chromatography–mass spectrometry metabolomics were used to identify contemporaneous and lagged associations between individual proteins/metabolites and subsequent changes in cardiac structure/function. The clinical significance is that multi-omics biomarkers may help predict or characterize cardiotoxicity-related cardiac injury in patients treated with anthracyclines and trastuzumab.
Ky B, Xia C, Ko K et al. · European heart journal · (2026) · View on PubMed ↗ · Free PDF ↗
Correlation between surrogate indicators of insulin resistance and all-cause mortality in patients with severe hemorrhagic stroke: a multicenter retrospective cohort study in the United States.
This multicenter retrospective cohort study in the United States evaluated correlations between surrogate indicators of insulin resistance and all-cause mortality in critically ill patients with severe hemorrhagic stroke admitted to the ICU. The key finding was that higher insulin-resistance surrogate measures were associated with increased all-cause mortality in this population. This is significant because it suggests insulin resistance may be a prognostic biomarker and potential therapeutic target in severe hemorrhagic stroke outcomes.
Zou D, Lin B, Wu B et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗
Targeting PHKA2 by Thymol alleviates sepsis induced cardiomyocyte pyroptosis via FOXA1/KLF4-mediated macrophage polarization.
This study tested whether thymol alleviates sepsis-induced cardiomyocyte pyroptosis by targeting PHKA2 and modulating FOXA1/KLF4-mediated macrophage polarization in a septic cardiomyopathy model. In a cecal ligation and puncture (CLP) mouse model, thymol reduced cardiomyocyte pyroptosis and linked the protective effect to PHKA2 inhibition and downstream FOXA1/KLF4 signaling that reprograms macrophage polarization. These findings identify PHKA2 and the FOXA1/KLF4 macrophage axis as mechanistic targets for developing adjunct therapies to mitigate sepsis-associated cardiac dysfunction.
Zhu H, Han S, Xue C et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
Cardiovascular disease: Lipids, atherosclerosis & vascular inflammation
Proteomic signatures as biomarkers of atherosclerosis burden.
This study aimed to derive plasma proteomic signatures that quantify systemic atherosclerosis burden using UK Biobank data. It trained machine-learning models on Olink Explore 3072 plasma proteomics (2,920 proteins) in a nested propensity-score-matched case-control sample (1,666 cases and 1,666 controls) to generate four AtheroBurden signatures, including one whole-proteome signature and three biologically informed subsets (genetically anchored, atherogenesis-related, and artery-enriched). The significance is that these circulating proteomic signatures could provide scalable biomarkers to detect and estimate atherosclerosis burden beyond imaging.
Zhang L, Omarov M, Xu L et al. · Cardiovascular research · (2026) · View on PubMed ↗
Immunomodulatory endothelial cells contribute to T cell recruitment and activation via antigen presentation on MHC II.
This study examined how immunomodulatory endothelial cells (IMEC) emerge under inflammation and how they interact with T cells via antigen presentation on MHC II. The key finding is that using flow cytometry and proteomics in vitro, supported by endothelial cell translatome/single-cell transcriptome analyses from murine atherogenesis and single-cell transcriptomes from human atherosclerotic arteries, IMEC contribute to T cell recruitment and activation through MHC II–dependent antigen presentation. The clinical/scientific significance is that IMEC–T cell antigen presentation provides a mechanistic pathway that could be targeted to modulate vascular inflammation in atherosclerosis and after myocardial infarction.
Cartura M, Aliraj B, Szymański W et al. · Cardiovascular research · (2026) · View on PubMed ↗
Biologics for cardiovascular diseases: from bench to bedside.
This review examined the translational landscape of biologics for cardiovascular diseases, including recombinant proteins, gene therapies, and cell therapies, and how they target processes such as lipid metabolism modulation. The key finding is that biologics are increasingly positioned to shift cardiovascular care from symptom control toward disease modification, including via lipid-related pathways. This is significant because it frames emerging therapeutic options for cardiovascular conditions that remain inadequately managed by traditional drugs.
Sun X, Wang X, Jia R et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Baicalein attenuates atherogenesis by suppressing endothelial pyroptosis via cylindromatosis-mediated tumor necrosis factor receptor-associated factor 6 deubiquitination.
This study examined whether baicalein (BAI) attenuates atherosclerosis by modulating endothelial pyroptosis, focusing on cylindromatosis (CYLD)-mediated deubiquitination of tumor necrosis factor receptor-associated factor 6 (TRAF6) in ApoE−/− mice and ox-LDL–stimulated HUVECs. BAI reduced endothelial pyroptosis and atherosclerotic pathology while mechanistically suppressing CYLD-dependent TRAF6 deubiquitination. The results support a specific CYLD–TRAF6 axis as a therapeutic target for anti-atherosclerotic interventions aimed at pyroptosis control.
Jiang Y, Sun Y, Li J et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
Metabolism & endocrine: Diabetes/obesity/GLP-1 & metabolic redox
Multiomics analysis of primary metabolism reveals the genetic basis of nitrogen partitioning modulated by ZmAVT1A-1 in maize.
This multiomics study integrated genomic, transcriptomic, and metabolomic data from 1,404 maize progenies derived from 24 diverse founders to identify causal genes controlling primary metabolism and nitrogen partitioning, focusing on ZmAVT1A-1. The authors prioritized ZmAVT1A-1, encoding a putative amino acid transporter, as a key regulator of amino acid accumulation, supported by natural variation and transgenic analyses. Scientifically, it provides a systems-level genetic basis for nitrogen partitioning and a candidate gene for improving maize nutritional quality.
Jin M, Yan S, Wu Y et al. · Nature genetics · (2026) · View on PubMed ↗
Joint effects of depression, lipid metabolic dysfunction, and their trajectories on incident cardiometabolic multimorbidity: a prospective multi-cohort analysis from two national cohorts.
This prospective multi-cohort analysis used individual-level data from CHARLS (China Health and Retirement Longitudinal Study) and ELSA (English Longitudinal Study of Ageing) to examine how depression and lipid metabolic dysfunction—and their trajectories—jointly predict incident cardiometabolic multimorbidity (CMM) in middle-aged and older adults. The key finding was that depression and lipid metabolic dysfunction show combined (joint) effects on CMM risk, and that co-trajectories over time further refine risk prediction. This is significant because it supports targeting modifiable mental-health and lipid-related factors to prevent or delay CMM in ageing populations.
Zeng Y, Wang Q, He H et al. · Lipids in health and disease · (2026) · View on PubMed ↗ · Free PDF ↗
Lipid Metabolic Disorders: a Pivotal Driver in Type 2 Diabetes Mellitus Pathogenesis.
This review synthesized evidence on how lipid metabolism disorders (e.g., elevated free fatty acids, triglycerides, and LDL-C with reduced HDL-C) contribute to type 2 diabetes mellitus (T2DM) pathogenesis, with emphasis on insulin resistance in normoglycemic obese individuals. It reports that dyslipidemia is a recurring mechanistic driver in the T2DM cascade and highlights emerging therapeutic strategies aimed at key nodes in this lipid-driven pathway. Clinically, the work supports precision management of T2DM by targeting specific lipid abnormalities rather than treating hyperglycemia alone.
Wu J, Wang H, Fu M et al. · Current obesity reports · (2026) · View on PubMed ↗ · Free PDF ↗
GLP-1 receptor agonists in pediatric obesity and diabetes: a systematic review of efficacy, metabolic effects, and safety.
This systematic review evaluated glucagon-like peptide-1 receptor agonists (GLP-1 RAs)—including semaglutide and liraglutide—in children and adolescents (age 6 to <18 years) with obesity or youth-onset type 2 diabetes mellitus, drawing on seven randomized controlled trials and six meta-analyses (901 participants). Semaglutide 2.4 mg/week showed the largest BMI reduction in adolescents with obesity, and liraglutide 3.0 mg/day also improved BMI standard deviation scores (BMI SDS). These findings support GLP-1 RA efficacy and safety as evidence-based pharmacotherapy options to complement lifestyle intervention and metformin in pediatric obesity/T2DM, while highlighting the need for ongoing long-term pediatric outcome data.
Soliman AT, Alyafei F, Khalil A et al. · Diabetes research and clinical practice · (2026) · View on PubMed ↗
Redox coupling of lactate and β-hydroxybutyrate: An inter-organ circuit linking metabolic flexibility, mitochondrial adaptation, and disease.
This study proposed a mechanistic framework for how lactate and β-hydroxybutyrate (βHB) act as redox-active metabolites forming a redox-coupled inter-organ circuit across liver, kidney, heart, and skeletal muscle. It links LDH- and BDH1-dependent reactions with monocarboxylate transport to coordinate cytosolic/mitochondrial NAD+/NADH redox states and enable metabolic flexibility during fasting, exercise, and hypoxia. The work advances understanding of metabolic adaptation and may inform redox-targeted strategies for diseases involving impaired fuel switching and mitochondrial dysfunction.
Lin D, Qiu X, Wang Y et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗
Apigenin ameliorates methionine-choline deficient diet-induced metabolic-associated fatty liver disease through modulation of gut microbiota-liver axis.
This study investigated whether apigenin ameliorates methionine-choline deficient (MCD) diet-induced metabolic-associated fatty liver disease (MAFLD) by modulating the gut microbiota–liver axis in mice. In the MCD model, apigenin improved MAFLD phenotypes and mechanistically linked these effects to changes in gut microbial composition and downstream host lipid metabolism pathways. The work supports apigenin as a potential gut-microbiota-targeted therapeutic candidate for MAFLD.
Xiong F, Xu Y, Wang X et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
[The role of obesity and weight reduction in obstructive sleep apnea].
This article reviewed the role of obesity and weight reduction in obstructive sleep apnea (OSA), focusing on how weight loss affects disease severity and cardiometabolic risk. It highlighted that weight reduction improves key outcomes such as the apnea–hypopnea index (AHI) and sleep architecture, and it discussed how current care models often underemphasize integrated weight management compared with positive airway pressure (PAP). The review also considers incretin-based therapies (e.g., GLP-1 receptor agonists and dual GLP-1/glucose-dependent insulinotropic polypeptide approaches) as potential adjuncts for OSA patients with obesity.
Horváth G, Berner SC, Bardóczi AB et al. · Orvosi hetilap · (2026) · View on PubMed ↗
5-methoxytryptamine improves hepatic inflammation and insulin resistance in a macrophage C-X-C motif chemokine ligand 14 dependent manner.
This study tested whether 5-methoxytryptamine (5MT) improves hepatic inflammation and insulin resistance in a macrophage C-X-C motif chemokine ligand 14 (CXCL14)–dependent manner in metabolic disease models. 5MT treatment ameliorated insulin resistance and hepatic steatosis in high-fat diet (HFD) and db/db mice, and the beneficial effects were linked to CXCL14-dependent signaling in macrophage-related pathways. The work supports 5MT as a candidate metabolic immunomodulator and positions CXCL14 as a mechanistic mediator of its insulin-sensitizing and anti-inflammatory effects.
Liao X, Xiao Y, Liu B et al. · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗
Efficacy and Safety of Pioglitazone Added to Metformin and SGLT2 Inhibitors in Type 2 Diabetes: An Updated Systematic Review and Meta-analysis.
This updated systematic review and meta-analysis evaluated the efficacy and safety of adding pioglitazone as a third-line therapy in type 2 diabetes mellitus (T2DM) patients inadequately controlled on metformin plus an SGLT2 inhibitor. The key finding was that pioglitazone add-on improved glycemic and cardiometabolic outcomes compared with control regimens, while also characterizing its safety profile across randomized controlled trials. Clinically, the results inform treatment intensification decisions for T2DM when metformin and SGLT2 inhibitors are insufficient.
Hussain SI, Jalal AA, Adnan Z et al. · The Annals of pharmacotherapy · (2026) · View on PubMed ↗
Aging, senescence & gerotherapeutics
Associations of proteomic age clocks with lifestyle risk factors, incident chronic diseases and mortality in two European cohorts.
This study assessed whether plasma SomaScan-based proteomic “age clocks” (including organ-specific clocks) predict lifestyle risk factors, 24 incident chronic diseases, and all-cause mortality in 17,473 participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, with replication in the Whitehall II study. A global proteomic age acceleration metric (“global age gap”) was associated with smoking, alcohol consumption, physical inactivity, and higher all-cause mortality. These findings support proteomic age clocks as clinically useful biomarkers linking modifiable lifestyle exposures to long-term chronic disease and mortality risk.
Robinson O, Xiao H, Homann J et al. · Nature aging · (2026) · View on PubMed ↗
ECMO for patients with obesity: evidence and practice.
This review studied how obesity affects patient selection, ECMO initiation, cannulation, anticoagulation, and monitoring in patients requiring veno-venous (VV) or veno-arterial (VA) extracorporeal membrane oxygenation (ECMO). It found that available (mostly retrospective) evidence—often using body mass index categories—suggests obesity meaningfully alters respiratory/cardiovascular physiology and drug pharmacokinetics and is associated with practical and outcome-relevant challenges during ECMO care. Clinically, the synthesis supports more careful, physiology- and pharmacokinetics-informed ECMO management and selection strategies for obese patients needing VV/VA ECMO.
Moyon Q, Hermans G, Abrams D et al. · Intensive care medicine · (2026) · View on PubMed ↗
Urinary protein vs albumin for assessing kidney failure risk in chronic kidney disease.
This study investigated whether urinary protein-to-creatinine ratio (UPCR) or urinary albumin-to-creatinine ratio (UACR) better predicts kidney failure risk in chronic kidney disease (CKD) using data from the Chronic Kidney Disease Japan Cohort. The key finding is that it compared the association of a 30% decrease in UPCR or UACR over 2 years with subsequent risk of kidney failure requiring replacement therapy (KFRT), aiming to clarify which surrogate endpoint is more informative than the other. The clinical significance is that it can inform routine CKD monitoring strategies by determining whether proteinuria (UPCR) or albuminuria (UACR) more reliably forecasts progression to kidney failure.
Toyama T, Imaizumi T, Hamano T et al. · Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · (2026) · View on PubMed ↗ · Free PDF ↗
Effectiveness of High-Intensity Versus Low-To-Moderate-Intensity Resistance Training in Improving Muscle Strength and Bone Mineral Density in Older Adults: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
This systematic review and meta-analysis studied randomized controlled trials comparing high-intensity resistance training (≥70% one-repetition maximum) versus low-to-moderate intensity (<70% 1RM) resistance training in older adults (age ≥50 years). The key finding is that across 18 trials (1283 participants), the analysis evaluated effects on lower-limb muscle strength and bone mineral density outcomes (including lumbar spine measures, per the truncated abstract). The clinical significance is that it helps define the optimal resistance-training intensity to improve sarcopenia- and osteoporosis-related outcomes in older adults.
Shen YC, Chen KH, Hou WH et al. · Geriatrics & gerontology international · (2026) · View on PubMed ↗
Dissolvable antimicrobial microneedles loaded with bone marrow mesenchymal stem cell-derived migrasomes for diabetes wound treatment.
This preclinical study developed dissolvable antimicrobial microneedles loaded with bone marrow mesenchymal stem cell (BMSC)-derived migrasomes (Migs) for diabetic wound treatment. The key finding was that migrasome-loaded microneedles address diabetic wound barriers—excess inflammation, impaired perfusion, elevated reactive oxygen species (ROS), and infection susceptibility—by leveraging the immunomodulatory and regenerative functions of migrasomes. This is significant because it combines localized, minimally invasive delivery with EV-subtype therapeutics to potentially improve healing in difficult-to-treat diabetic wounds.
Zhao R, Chen S, Zhou L et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗
Preventing post-denosumab bone loss with zoledronate: a 2-year randomized trial in post-menopausal women without and with pre-exposure to bisphosphonates.
This multicenter randomized open-label trial studied zoledronate timing and dosing to prevent post-denosumab bone loss in 44 post-menopausal women after long-term denosumab use, stratified by prior bisphosphonate exposure. The key finding was that early and multiple zoledronate infusions are needed to preserve bone mineral density after stopping denosumab, with prior bisphosphonate history influencing outcomes. Scientifically and clinically, it provides evidence-based guidance to reduce rebound bone loss and fracture risk following denosumab discontinuation.
Ferrari S, Hars M, Biver E et al. · Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · (2026) · View on PubMed ↗ · Free PDF ↗
From Lifespan Extension to Hallmark-Informed Gerotherapeutic Prioritization: A Bibliometric-Guided, Strategy-Oriented Review of Anti-Aging Drug Research.
This bibliometric-guided strategy-oriented review mapped anti-aging drug research from 2005–2025 and assessed translational readiness using hallmark-informed frameworks. The key finding is that the field converges on three partially overlapping intervention axes: senotherapeutics targeting cellular senescence/SASP, nutrient-sensing/metabolic gerotherapeutics (mTOR/AMPK/autophagy/mitochondrial adaptation), and homeostasis-related approaches. This is significant for prioritizing gerotherapeutic candidates by aligning mechanistic evidence with translational feasibility.
Liu Z, Abulaiti A, Li D et al. · Ageing research reviews · (2026) · View on PubMed ↗ · Free PDF ↗
Sulfhydrated TFEB alleviates blast-induced lung injury by maintaining epithelial barrier integrity through the IGF2R/MMP-2/9 pathway.
This study investigated whether sulfhydrated TFEB (Transcription Factor EB) protects against blast-induced lung injury (BLI) by preserving epithelial barrier integrity via the IGF2R/MMP-2/9 signaling pathway, and tested a hydrogen sulfide (H2S)-releasing nanozyme (Pt@Pd-S) as a therapeutic intervention. Using bioinformatic analysis of single-cell RNA sequencing (scRNA-seq) data and mechanistic experiments, it identified TFEB activation and the IGF2R→MMP-2/9 axis as key regulators of barrier integrity during BLI, with Pt@Pd-S providing therapeutic benefit through this pathway. These results suggest TFEB sulfhydration and the IGF2R/MMP-2/9 cascade as actionable targets for translational treatment of BLI.
Du JK, Luo CJ, Zhan JH et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗
Comparative effectiveness of oral cooling and moisturizing interventions for managing postoperative thirst in post-anesthesia care unit patients: A systematic review and network meta-analysis.
This systematic review and network meta-analysis compared oral cooling versus moisturizing interventions for relieving postoperative thirst in post-anesthesia care unit (PACU) patients. Across studies identified from PubMed, Web of Science, CINAHL, EMBASE, and Scopus (to January 16, 2026), it synthesized relative effectiveness of different nonpharmacologic thirst-relief strategies. The findings can guide evidence-based selection of the most effective bedside interventions to reduce patient discomfort and potential adverse effects after anesthesia.
Lin JY, Hsieh CC, Chen SR et al. · International journal of nursing studies · (2026) · View on PubMed ↗
Prebiotic Supplementation in Celiac Disease: A Systematic Review of Clinical Efficacy, Safety, and Nutritional Outcomes.
This systematic review evaluated the clinical efficacy, safety, and nutritional outcomes of prebiotic supplementation in patients with celiac disease (CD) despite adherence to a gluten-free diet. Across included clinical studies, prebiotics were assessed for effects on persistent symptoms and nutrient deficiencies, with outcomes synthesized according to PRISMA-guided evidence selection. The review helps clarify whether prebiotics can serve as an effective and safe adjunct to gluten-free diet management in CD and identifies evidence gaps for future trials.
Shahzil M, Irfan MZ, Kazmi SK et al. · Journal of gastrointestinal and liver diseases : JGLD · (2026) · View on PubMed ↗ · Free PDF ↗
Explaining inequalities in quality of life: a longitudinal study of health disparities in Norway.
This longitudinal study used Norwegian Tromsø Study data to examine how health disparities in quality of life develop over time and which socioeconomic and behavioral factors explain them in adults aged 25–54 followed for 21 years. It aimed to move beyond single-indicator cross-sectional analyses by integrating broader sets of socioeconomic and health behavior variables to better explain later-adulthood quality-of-life inequalities. The findings are intended to inform more effective, behavior- and context-sensitive approaches to reducing health disparities.
Olsen JA, Chen G, Løvsletten O · Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation · (2026) · View on PubMed ↗ · Free PDF ↗
Bio-hybrid nanovesicles with multimodal antioxidant and immunomodulatory functions attenuate acute kidney injury.
This work studied bio-hybrid nanovesicles (ES-EVs) engineered by incorporating epigallocatechin-3-gallate (EGCG) nanoparticles and selenomethionine (SeMet) into extracellular vesicles derived from human umbilical sources to treat acute kidney injury (AKI). ES-EVs attenuated AKI by simultaneously reducing oxidative stress (reactive oxygen species burden) and modulating inflammatory immune responses. The integrated antioxidant–immunomodulatory nanovesicle strategy suggests a multifunctional therapeutic platform for AKI that targets both tubular injury and inflammation.
Chen W, Yuan H, Liu H et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗
Removal of aging microenvironment of bone defects can effectively promote bone defect repair.
This study investigated whether removing the aging microenvironment in bone defects improves bone repair, focusing on how a senescent vascular niche after injury affects mesenchymal stem cell (MSC) proliferation and differentiation in a rat femoral trochlear defect model. The authors report that clearing the senescent/aging niche enhances MSC regenerative performance and promotes bone defect healing, implicating mechanisms tied to the senescent vascular environment. These results suggest that targeting age-related microenvironmental dysfunction could improve MSC-based therapies for orthopedic bone defects.
Huang J, Long H, Malik MA et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Chlorogenic acid attenuates skin senescence and UVR-induced photoaging via the modulation of mitochondrial function.
This study evaluated chlorogenic acid (CGA) as a modulator of mitochondrial function to attenuate skin senescence and UVR-induced photoaging in human dermal fibroblasts and human epidermal keratinocytes. The key finding is that CGA improves mitochondrial function and reduces senescence/photoaging phenotypes, with collagen I production and mitochondrial readouts used to support the mechanism. These results are significant because they position CGA’s mitochondrial modulation as a mechanistic basis for anti-aging interventions against UV-induced skin damage.
Li R, Hu C, Zhou P et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Generated automatically on June 30, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.