Diabetic cardiomyopathy (DCM) is a common complication associated with diabetes. The (
pro)renin receptor (PRR) is an important member of the local tissue renin-angiotensin system and plays a vital role in many
cardiovascular diseases. Yes-associated
protein (YAP) also plays a crucial role in many
cardiovascular diseases. However, the mechanism responsible for the effects of PRR and YAP on DCM remains unclear. The purpose of this study was to determine the role of PRR in the pathological progression of DCM and whether PRR influences the
pathological processes of
diabetic cardiomyopathy through YAP. We first established
diabetic cardiomyopathy rats model, downregulated the expression of PRR, and upregulated and downregulated the expression of YAP. The levels of myocardial
inflammation and
fibrosis were then measured and cardiac function was evaluated. In vitro, primary rat cardiac fibroblasts (CFs) were cultured with high
glucose, with or without transfection with recombinant adenovirus expressing PRR, and
GSK621 was used to observe the effect of AMPK. The levels of
inflammation and
fibrosis were measured in vitro. The results showed that PRR and YAP silencing alleviated myocardial
inflammation and
fibrosis.
GSK621 blocked the effect of PRR on AMPK and YAP and improved CF
inflammation and
fibrosis. The inhibition of PRR expression offers a new therapeutic strategy for the treatment of DCM. The effects of PRR on the pathological process of DCM in rats may be mediated via the PRR-AMPK-YAP pathway.