ArticleJACC. Basic to translational science2024
Deubiquitinase USP25 Alleviates Obesity-Induced Cardiac Remodeling and Dysfunction by Downregulating TAK1 and Reducing TAK1-Mediated Inflammation.
Article in JACC. Basic to translational science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed.
- Review
- BCKDK protects against obesity-induced cardiac remodelling and dysfunction by alleviating mitochondrial oxidative stress and ROS-driven MAPK signalling.Redox biology · 2026Article
- VCPIP1 drives diabetic cardiomyopathy by deubiquitinating AMPKγ1 and preventing AMPKα-γ subunit assembly in cardiomyocytes.Signal transduction and targeted therapy · 2026Article
- Chaperone-Mediated Autophagic Degradation of USP9X in Macrophages Exacerbates Postmyocardial Infarction Inflammation and Cardiac Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- USP25 deficiency suppresses diet-induced obesity via ubiquitination and degradation of PARP1 and Elovl3 downregulation.Journal of lipid research · 2026Article
- Ubiquitin-specific protease 25: a new regulator for cardiovascular and cerebrovascular diseases.Frontiers in cell and developmental biology · 2026Review
- Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 and inducing mitochondrial dysfunction.Nature communications · 2025Article
- Obesity accelerates cardiovascular ageing.European heart journal · 2025Review
- Emerging Role of Targeting Deubiquitinating Enzymes to Inhibit Pathological Cardiac Hypertrophy.Journal of the American Heart Association · 2025Article
- Targeting USP25 in the Heart: A Promising Therapeutic Strategy for Obesity-Associated Heart Disease?JACC. Basic to translational science · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deubiquitinating enzymes play a vital role in cardiovascular diseases. This study found that cardiomyocyte ubiquitin-specific protease 25 (USP25) expression was downregulated both in myocardial tissue of obesity cardiomyopathy and palmitic acid-stimulated cardiomyocytes. USP25 deficiency exacerbated high-fat diet-induced ventricular remodeling in mice, whereas overexpression of USP25 in cardiomyocytes reversed this pathological phenotype. Mechanistically, USP25 directly binds to TAK1 and P62, and the 178-cysteine of USP25 removes the K63 ubiquitin chain from P62, which promotes the degradation of TAK1 through the autophagy-lysosome pathway, thereby ameliorating obesity-induced ventricular remodeling by reducing inflammation through the TAK1-MAPK pathway. This finding identifies USP25 as a potential therapeutic target for obesity cardiomyopathy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.