TRPC3 and Myocardial fibrosis: In cardiac hypertrophy caused by mechanical stress, the activation of TRPC3 leads to a significant increase in reactive oxygen species (ROS) production, and the activation of Rho-associated kinase (RhoA) in cardiomyocytes and fibroblasts, resulting in interstitial fibrosis, while the deletion of Trpc3 gene has an inhibitory effect on myocardial fibrosis (Kitajima et al., 2016).