Cardiac aging is driven by reduced autophagy, mitochondrial oxidative stress, and telomere attrition, leading to structural and functional changes across the heart and vasculature.
As the elderly segment of the world population increases, it is critical to understand the changes in cardiac structure and function during the normal aging process. In this review, we outline the key molecular pathways and cellular processes that underlie the phenotypic changes in the heart and vasculature that accompany aging. Reduced autophagy, increased mitochondrial oxidative stress, telomere attrition, altered signaling in insulin-like growth factor, growth differentiation factor 11, and 5'- AMP-activated protein kinase pathways are among the key molecular mechanisms underlying cardiac aging. Aging promotes structural and functional changes in the atria, ventricles, valves, myocardium, pericardium, the cardiac conduction system, and the vasculature. We highlight the factors known to accelerate and attenuate the intrinsic aging of the heart and vessels in addition to potential preventive and therapeutic avenues. A greater understanding of the processes involved in cardiac aging may facilitate our ability to mitigate the escalating burden of CVD in older individuals and promote healthy cardiac aging.
Obas et al. (Mon,) conducted a review in Cardiac aging. Cardiac aging is driven by reduced autophagy, mitochondrial oxidative stress, and telomere attrition, leading to structural and functional changes across the heart and vasculature.
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