AGT and Myocardial fibrosis: For example, the activation of angiotensin II (Ang-II) can promote the norepinephrine (NE) release and increase the excitability of α1 receptor, lead to the myocardial fibrosis, hypertrophy, and deformation through activating the proto-oncogene expression, increasing the synthesis of proteins and microRNAs and regulating the function of mRNAs in cardiomyocytes [37].