Role of Impaired Mitochondrial Autophagy in Cardiac Aging: Mechanisms and Therapeutic Implications

Advanced age per se is a major risk factor for cardiovascular disease (CVD). Apart from the chronic exposure to known cardiovascular risk factors, intrinsic aging of the cardiovascular system amplifies the vulnerability to various stressors, ultimately favoring the development of CVD in late life. The process of cardiac aging involves derangements in multiple cellular pathways. Among these, impairments in mitochondrial function arising from failure of mitochondrial quality control are considered to be a major contributing factor to heart senescence. Besides being less bioenergetically efficient, damaged mitochondria produce larger amounts of reactive oxygen species and are more prone to induce apoptosis. This results in oxidative damage to cardiomyocyte components and dismissal of postmitotic and virtually irreplaceable cardiac cells. The chapter summarizes the current knowledge about prominent mechanisms and consequences of mitochondrial decay and failure of mitochondrial quality control in the context of cardiac aging. The therapeutic potential of targeting specific mitochondrial pathways is also discussed.