We, therefore, conclude that the aging process increases the production of oxidative stress (the suppression of SOD2 and an increase in TBARS levels along with protein carbonyl content), and the increase in oxidative stress upregulates the expression of the aging marker (the expression of p53) as well as induces tissue remodeling (the disarray of cardiomyocytes, the enlargement of intercellular space, and the deposition of collagen), resulting in heart failure. The gene discussed is SOD2; the disease is heart failure.