Abstract 13310: Sulfiredoxin Ameliorates Oxidative Stress-Induced Cardiomyocyte Apoptosis and Mitochondrial Dysfunction by Inhibiting Oxidation of Peroxiredoxin 3

BackgroundOxidative stress is intimately involved in cardiac injury including apoptosis. Peroxiredoxin3 (Prx3) reduces H2O2 in mitochondria and exerts a protective effect against cardiac remodeling. Sulfiredoxin (Srx), an antioxidant protein, exclusively reduces oxidized Prxs. The purpose of this study was to investigate whether Srx plays a protective role against oxidative stress-induced cardiac injury by inhibiting oxidation of Prx3.Methods and ResultsTransverse aortic constriction (TAC) or sham operation was performed in C57BL/6 mice. TAC-operated mice exhibited cardiac hypertrophy by 7 days and cardiac systolic dysfunction by 28 days. At 7 days, Srx protein levels were increased in TAC-operated mouse hearts compared with baseline by 140% (p