Angiotensin II (AngII) can promote ROS synthesis by cardiomyocyte mitochondria, resulting in loss of mtDNA and increased autophagy (Dai et al., 2011b) In a mouse model of catalase overexpression, an antioxidant polypeptide that specifically targets the mitochondria (SS-31) can reduce myocardial damage, inhibit cardiac hypertrophy and fibrosis, and reverse the mitochondrial damage caused by Ang-II. Here, AGT is linked to cardiac hypertrophy.