Aging is characterized by a progressive decline in cardiac function. A critical contributor to the age-related impairment in cardiac function is the loss of cardiac myocytes through “apoptosis”, or programmed cell death. Structural remodeling in the heart with advancing age includes (a) loss of cardiomyocytes, (b) reactive hypertrophy of the remaining cardiomyocytes, and (c) increased connective tissue and altered geometry. The loss of cardiomyocytes with aging occurs through apoptosis. Particularly, mitochondrial-mediated apoptotic pathway is the best characterized and believed critical in regulating apoptosis with aging, suggesting that mitochondria are very important sites of programmed cell death. It has been also reported that mitochondrial dysfunction, oxidative stress, and impaired stress response contribute to age-induced mechanical remodeling as well as apoptosis. In contrast, exercise training not only improves cardiac function, but also reduces the risk of heart disease. We recently found that aging increased mitochondrialmediated apoptotic signaling and apoptosis in the left ventricle, while chronic exercise training was effective in diminishing mitochondrial- mediated apoptotic signaling pathways in the aging heart, as indicated by lower DNA fragmentation, terminal deoxynucleotidyl transferase- mediated dUTP nick end labeling (TUNEL)-positive staining, and caspase-3 cleavage, when compared with left ventricles from the agematched sedentary group. In this review, we will provide a comprehensive update regarding the effects of aging and exercise training on apoptosis in the heart.
APOPTOSIS AND MITOCHONDRIAL CONTROL
AGING AND APOPTOSIS
APOPTOSIS AND HEART
EXERCISE AND APOPTOSIS IN THE AGING HEART
CONFLICT OF INTEREST