Abstract
Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult. Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Aging and cardiac pathologies are also associated with increased senescence in the heart. However, the cause and consequences of cardiac senescence during aging or in cardiac pathologies are mostly unrecognized. Further, despite recent advancement in anti-senescence therapy, the targeted cell type and the effect on cardiac structure and function have been largely overlooked. The unique cellular composition of the heart, and especially the functional properties of cardiomyocytes, need to be considered when designing therapeutics to target cardiac aging. Here we review recent findings regarding key factors regulating cell senescence, mitochondrial health as well as cardiomyocyte rejuvenation.
Highlights
Aging is associated with progressive functional deterioration at both organ and cellular level [1]
With the increased understanding of the features of senescence, it is typically classified in two categories [9,11]: (1) replicative senescence that occurs during natural aging and is induced in part by the erosion of telomerase due to cell cycle progression, and (2) stress-induced premature senescence (SIPS), seen in response to cytotoxic stresses such as anti-cancer therapy [12]
As the demography shift into an older population [1], it is imperative to advance our knowledge of aging to dissect its role from diseases
Summary
Aging is associated with progressive functional deterioration at both organ and cellular level [1]. With the increased understanding of the features of senescence, it is typically classified in two categories [9,11]: (1) replicative senescence that occurs during natural aging and is induced in part by the erosion of telomerase due to cell cycle progression, and (2) stress-induced premature senescence (SIPS), seen in response to cytotoxic stresses such as anti-cancer therapy [12] While both replicative senescence and SIPS likely contribute to cardiac aging, SIPS probably pertains a more critical role in driving CM aging as the CMs have little capacity for cell cycle but higher mitochondrial mass rendering them susceptible to mitochondrial dysfunction and increased ROS [5]. We review recent data on factors regulating cardiac aging with focus on non-coding RNAs and their role in regulating mitochondrial function (Figure 1)
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