ArticleScience advances2025
Cardiomyocyte-derived YOD1 promotes pathological cardiac hypertrophy by deubiquitinating and stabilizing STAT3.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- The deubiquitinase YOD1 in renal tubular epithelial cells promotes diabetic kidney disease by stabilizing KEAP1.Acta pharmacologica Sinica · 2026Article
- Microglial Deubiquitinase OTUD7B Stabilizes STAT3 to Promote Neuroinflammation and Cognitive Decline in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Astragaloside IV Reduces Sorafenib-Induced Cardiotoxicity by Inhibiting Apoptosis Through the STAT3/HIF-1α/Bcl-2 Signaling Pathway.International journal of molecular sciences · 2026Article
- Cardiomyocyte-derived OTUD7B promotes cardiac hypertrophy by deubiquitinating SERCA2a.Theranostics · 2026Article
- YOD1 drives acute kidney injury by deubiquitinating Bax and promoting apoptosis in tubular epithelial cells.Theranostics · 2026Article
- Qingda granule prevents Ang II-induced cardiac hypertrophy via inhibiting NF-κB signaling pathway.Frontiers in pharmacology · 2025Article
- Ubiquitination-mediated protein homeostasis in cardiovascular diseases: molecular mechanisms and therapeutic opportunities.American journal of cardiovascular disease · 2025Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identifying previously unknown targets for pathological cardiac hypertrophy and understanding its mechanisms are crucial. Here, we observed that the deubiquitinating enzyme YOD1 was moderately elevated in human hypertrophic myocardium and mouse models. Cardiomyocyte-specific knockout of YOD1 reduced Ang II- and TAC-induced cardiac hypertrophy. Subsequently, we used multiple proteomic analyses to identify and confirm STAT3 as a substrate protein for YOD1. Mechanistically, our findings revealed that the C155 site of YOD1 removes K48-linked ubiquitin chains from K97 on STAT3, stabilizing STAT3 levels and enhancing its nuclear translocation in cardiomyocytes under Ang II stimulation. Notably, inhibiting STAT3 reversed the antihypertrophic effects of YOD1 deficiency in Ang II-challenged mice. In addition, pharmacological inhibition of YOD1 mitigated Ang II-induced pathological ventricular remodeling in mice. This study clarifies the role of YOD1 and introduces a previously unidentified YOD1-STAT3 axis in regulating pathological cardiac hypertrophy, providing valuable insights for drug development targeting this condition.
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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 Socratic graph.