Targeting STK39 ameliorates cardiac remodeling by Improving Mitochondrial function through degradation of IFIT3

In this study, we identified serine/threonine kinase 39 (STK39) as a key mediator, showing that it is significantly upregulated in human hypertrophic hearts and in the hearts of mice after transverse aortic constriction.

Cardiomyocyte-specific knockdown of STK39 can improve cardiac hypertrophy, enhance ventricular function, and reduce myocardial fibrosis in vivo, while in vitro, silencing STK39 in mouse cardiomyocytes can inhibit angiotensin II (Ang II)-induced hypertrophic growth, fibrosis, and mitochondrial dysfunction. Therefore, RNA sequencing was performed on cardiomyocytes from the AngII-siNC group and the AngII-siSTK39 group to identify downstream targets of STK39 and elucidate its signaling pathway mechanisms.