CD9 exacerbates pathological cardiac hypertrophy through regulating GP130/STAT3 signaling pathway

CD9 is a member of the tetraspanin protein family, which has been widely studied in inflammation cer, but not in pathological cardiac hypertrophy. In this study, we found that the expression of increased in transaortic constriction (TAC) myocardial tissue. Knockdown of CD9 alleviated damage cardiac function in the TAC model and reduced heart weight, cardiomyocyte size, and degree of and vice versa. Mechanistically, co-immunoprecipitation results showed that CD9 and GP130 can each other in cardiomyocytes, and knockdown of CD9 can reduce the protein level of GP130 and the phorylation of STAT3 in vivo and in vitro, and vice versa. GP130 knockdown reversed the aggravating fects of CD9 on pathological cardiac hypertrophy. Therefore, we conclude that CD9 exacerbates logical cardiac hypertrophy by regulating the GP130/STAT3 signaling pathway and may serve for cardiac