Circulation. 2003;107:490-497
doi: 10.1161/01.CIR.0000048894.99865.02
doi: 10.1161/01.CIR.0000048894.99865.02
(Circulation. 2003;107:490.)
© 2003 American Heart Association, Inc.
Special Review: Clinical Cardiology: New Frontiers |
Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises
Part III: Cellular and Molecular Clues to Heart and Arterial Aging
From the Gerontology Research Center, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Md.
Correspondence to Edward G. Lakatta, MD, National Institute on Aging, Intramural Research Program, Gerontology Research Center, Laboratory of Cardiovascular Science, 5600 Nathan Shock Dr, Baltimore, MD 21224-6825. E-mail lakattae@grc.nia.nih.gov
Key Words: aging • calcium • cardiovascular diseases • endothelium • remodeling
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Evidence supporting the hypothesis that age-associated changes in cardiovascular structure/function are implicated in the markedly increased risk for cardiovascular disease in older persons has been presented in the preceding 2 articles in this series.1,2 It follows that therapies to prevent or delay cardiovascular changes that accompany aging may reduce the risk for age-associated cardiovascular diseases. Understanding the nature and effectiveness of such therapies, however, requires an understanding of heart and arterial aging at the cellular and molecular levels. Fortunately, many of the age-associated changes in cardiac and arterial structure or function that have been observed in humans also occur across a wide range of other species. Insights gained from cellular and molecular studies in these animal models may hold clues that will assist in directing future efforts toward developing novel therapies for age-associated arterial and cardiac structural and functional remodeling in humans.
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Vascular Aging |
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Age-associated remodeling of the walls of large arteries of rodents (Table 1) and nonhuman primates is quite similar to that observed in humans and includes luminal dilation, intimal and medial thickening (Figure 1), vascular stiffening, and endothelial dysfunction.3–7
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