Reactive oxygen species are important downstream signaling factors for angiotensin II-mediated myocardial fibrosis; they can promote myocardial fibrosis by regulating TGF-β expression, which affects extracellular matrix (ECM) homeostasis and induces autophagy, thereby contributing to differentiation and proliferation of cardiac fibroblasts into myofibroblasts (Shi et al., 2015). This evidence concerns the gene AGT and Myocardial fibrosis.