ArticleResearch (Washington, D.C.)2025
USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377.
Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Post-translational modifications of mitochondrion-related proteins: integrative orchestrators of cell fate networks in cardiovascular disease.Cell communication and signaling : CCS · 2026Review
- 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
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Abstract
Alcoholic cardiomyopathy (ACM) is a type of dilated cardiomyopathy unrelated to ischemia, which develops as a consequence of chronic alcohol consumption. While ethanol-induced irreversible cardiomyocyte death is implicated in ACM development and progression, the precise molecular mechanisms involved are still obscure. In the current study, we demonstrate that ethanol exposure promotes receptor-interacting serine/threonine-protein kinase 1 (RIPK1) autophosphorylation and enhances pRIPK1-associated apoptosis and necroptosis in ACM models both in vivo and in vitro. Through co-immunoprecipitation (Co-IP) combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, we identified ubiquitin-specific protease 53 (USP53) as a pivotal deubiquitinase involved in modulating RIPK1 activation following ethanol stimulation in cardiomyocytes. Mechanistically, we found that ethanol induced up-regulation of USP53 via transcriptional induction by early growth response 1 (EGR1). Subsequently, USP53 interacted with the intermediate domain of RIPK1 and removed K63-linked ubiquitination at lysine-377 (K377), facilitating RIPK1 phosphorylation and triggering downstream apoptotic and necroptotic pathways in cardiac cells. Further, alcohol-fed cardiomyocyte-specific USP53 knockout (USP53
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Registered trials
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