Journal
ANNUAL REVIEW OF PHYSIOLOGY, VOL 80
Volume 80, Issue -, Pages 27-48Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021317-121454
Keywords
cardiovascular disease; atherosclerosis; vascular calcification; heart failure; prelamin A/lamin A; progerin
Categories
Funding
- Red de Investigacion Cardiovascular at ISCIII
- Progeria Research Foundation [2014-52]
- MEIC
- Pro-CNIC Foundation
- Severo Ochoa Center of Excellence (MEIC) [SEV-2015-0505]
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Aging, the main risk factor for cardiovascular disease (CVD), is becoming progressively more prevalent in our societies. A better understanding of how aging promotes CVD is therefore urgently needed to develop new strategies to reduce disease burden. Atherosclerosis and heart failure contribute significantly to age-associated CVD-related morbimortality. CVD and aging are both accelerated in patients suffering from Hutchinson-Gilford progeria syndrome (HGPS), a rare genetic disorder caused by the prelamin A mutant progerin. Progerin causes extensive atherosclerosis and cardiac electrophysiological alterations that invariably lead to premature aging and death. This review summarizes the main structural and functional alterations to the cardiovascular system during physiological and premature aging and discusses the mechanisms underlying exaggerated CVD and aging induced by prelamin A and progerin. Because both proteins are expressed in normally aging non-HGPS individuals, and most hallmarks of normal aging occur in progeria, research on HGPS can identify mechanisms underlying physiological aging.
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