Key result
Telomere shortening and dysfunction drive the pathogenesis of hypertension, atherosclerosis, and heart failure.
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Telomeres-the specialized DNA-protein structures at the ends of eukaryotic chromosomes-are essential for maintaining genome stability and integrity and for extended proliferative life span in both cultured cells and in the whole organism. Telomerase and additional telomere-associated proteins are necessary for preserving telomeric DNA length. Age-dependent telomere shortening in most somatic cells, including vascular endothelial cells, smooth muscle cells, and cardiomyocytes, is thought to impair cellular function and viability of the aged organism. Telomere dysfunction is emerging as an important factor in the pathogenesis of hypertension, atherosclerosis, and heart failure. In this Review, we discuss present studies on telomeres and telomere-associated proteins in cardiovascular pathobiology and their implications for therapeutics.
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Serrano et al. (2004) conducted a review in Cardiovascular disease (hypertension, atherosclerosis, and heart failure). Telomere dysfunction and telomere-associated proteins was evaluated on Cardiovascular pathobiology (hypertension, atherosclerosis, and heart failure). Telomere dysfunction and age-dependent shortening are emerging factors in the pathogenesis of hypertension, atherosclerosis, and heart failure (narrative review; no quantitative outcomes reported).
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