Consistent with a role for cardiomyocyte NOX4 in the maladaptation of the heart to RAAS hyperactivation, the treatment of mice with a mitochondrial-targeted antioxidant peptide prevented the upregulation of Nox4 and mitochondrial oxidative stress, as well as ameliorated cardiac hypertrophy, fibrosis, and diastolic dysfunction in response to AngII [64]. This evidence concerns the gene AGT and cardiac hypertrophy.