Under pathological conditions such as myocardial injury and hypertension, the key RAAS effector molecule angiotensin II (Ang II) mediates signal transduction via the AT1A receptor, upregulating the expression of fetal genes, collagen, and TGF-β1 in non-infarcted regions, thereby promoting left ventricular dilation, fibrosis, and dysfunction, and accelerating ventricular remodeling and HF progression (13). This evidence concerns the gene AGT and hypertensive disorder.