Western societies are rapidly aging, and cardiovascular diseases are the leading cause of death. In fact, age and cardiovascular diseases are positively correlated, and disease syndromes affecting the heart reach epidemic proportions in the very old. Genetic variations and molecular adaptations are the primary contributors to the onset of cardiovascular disease; however, molecular links between age and heart syndromes are complex and involve much more than the passage of time. Changes in CM (cardiomyocyte) structure and function occur with age and precede anatomical and functional changes in the heart. Concomitant with or preceding some of these cellular changes are alterations in gene expression often linked to signalling cascades that may lead to a loss of CMs or reduced function. An understanding of the intrinsic molecular mechanisms underlying these cascading events has been instrumental in forming our current understanding of how CMs adapt with age. In the present review, we describe the molecular mechanisms underlying CM aging and how these changes may contribute to the development of cardiovascular diseases.
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Review Article| June 24 2011
Molecular mechanisms of cardiomyocyte aging
Daniel R. Riordon;
Kenneth R. Boheler
1Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, U.S.A.
Correspondence: Dr Kenneth R. Boheler (email firstname.lastname@example.org).
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Anna Sheydina, Daniel R. Riordon, Kenneth R. Boheler; Molecular mechanisms of cardiomyocyte aging. Clin Sci (Lond) 1 October 2011; 121 (8): 315–329. doi: https://doi.org/10.1042/CS20110115
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