Cardiomyocyte-derived OTUD7B promotes cardiac hypertrophy by deubiquitinating SERCA2a.

ABSTRACT: Rationale: Pathological cardiac hypertrophy, triggered by persistent neurohumoral or hemodynamic stress, is a key precursor of ventricular dysfunction and heart failure. Deubiquitinating enzymes (DUBs) have emerged as critical regulators of cardiovascular biology. This study examined the function of a DUB, ovarian tumor domain-containing 7B (OTUD7B), in cardiac hypertrophy. Methods: Cardiomyocyte-specific OTUD7B knockout and overexpression mouse models were generated to evaluate myocardial hypertrophy and cardiac dysfunction in response to angiotensin II (Ang II) infusion or transverse aortic constriction (TAC). Quantitative ubiquitinome analysis, site-directed mutagenesis, and co-immunoprecipitation assays were performed to explore the substrate and mechanism of OTUD7B. R

SUBMITTER: Huang Z 

PROVIDER: S-EPMC12906209 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature