OTUD1 knockout significantly protected mice against angiotensin II- and transverse aortic constriction-induced cardiac dysfunction, hypertrophy, and fibrosis by modulating STAT3 activity.
Does OTUD1 promote pathological cardiac remodeling and heart failure by targeting STAT3 in cardiomyocytes?
OTUD1 promotes pathological cardiac remodeling and heart failure by deubiquitinating STAT3, suggesting OTUD1 as a potential therapeutic target for hypertensive heart failure.
Cardiomyocyte OTUD1 promotes pathological cardiac remodeling and dysfunction by deubiquitinating STAT3. These studies have highlighted a novel role of OTUD1 in hypertensive heart failure and identified STAT3 as a target of OTUD1 in mediating these actions.
Wang et al. (2023) studied Heart failure and cardiac remodeling. OTUD1 knockout vs. Wild-type mice was evaluated on Cardiac dysfunction, hypertrophy, and fibrosis induced by Ang II or TAC. OTUD1 knockout significantly protected mice against angiotensin II- and transverse aortic constriction-induced cardiac dysfunction, hypertrophy, and fibrosis by modulating STAT3 activity.