Reactive oxygen species(ROS) in the cardiac muscle are increased in cardiovascular diseases such as hypertension,coronary heart disease and heart failure.Oxidative stress mediates myocyte hypertrophy,myocyte apoptosis and interstitial fibrosis.And these changes are particularly pronounced in elderly patients or senescent animal disease models.The major sources of ROS in myocardium are mitochondria and the reduced nicotinamide adenine dinucleotide phosphate(NADPH) oxidase.Specific ROS such as hydrogen peroxide play an important role in myocardial remodeling in heart failure.Oxidative modifications of calcium handling proteins result in reduction of their activities,leading to decreased myocardial contractility.Reduction of oxidant levels and inhibition of oxidative modifications of specific proteins through inhibiting ROS sources may provide new strategies for the treatment of myocardial remodeling.

Cardiomyocyte autophagy plays an important role in maintaining normal cardiac structure and function.Recent studies have shown that cardiomyocyte autophagy is decreased in the aging heart.The expression of autophagy-related genes Atg5, Atg7 and Beclin1 decreases in the aging myocardium.Decreased cardiomyocyte autophagy in the aging heart is associated with dysregulation of phosphatidylinositol-3-kinase(PI3K)/serine-threonine kinase(Akt)/mammalian target of rapamycin(mTOR), adenosine monophosphate-activated protein kinase(AMPK)and/or the SIRT1 signaling pathways.In addition, reactive oxygen species and some neural hormonal factors such as endothelin-1 can also mediate the decrease of cardiomyocyte autophagy in cardiac aging.The regulation of cardiomyocyte autophagy may provide new strategies for the prevention and treatment of cardiomyopathy in the elderly.