USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377

) mice exhibited improved survival rates and less cardiomyocyte death in hearts compared with the control group. Our study identifies USP53 as a novel regulator of RIPK1-dependent cell death and advances our understanding of the mechanistic pathways of ACM. These results highlight the USP53-RIPK1 signaling axis as a potential therapeutic target for mitigating ACM progression.