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(Circulation Research. 2007;101:13.)
© 2007 American Heart Association, Inc.

Reviews

Mechanisms of Cardiovascular Disease in Accelerated Aging Syndromes

Brian C. Capell, Francis S. Collins, Elizabeth G. Nabel

From the Genome Technology Branch (B.C.C., F.S.C., E.G.N.), National Human Genome Research Institute; and National Heart, Lung, and Blood Institute (E.G.N.), NIH, Bethesda, Md.

Correspondence to Elizabeth G. Nabel, MD, National Heart, Lung, and Blood Institute, NIH, Building 31, Room 5A48, 31 Center Dr, MSC 2486, Bethesda, MD 20892-2486. E-mail nabele{at}nih.gov

This Review is part of a thematic series on Biological Role of Senescence in Cardiovascular Disease, which includes the following articles:

Telomere Biology and Cardiovascular Disease

Vascular Cell Senescence: Contribution to Atherosclerosis

Stem Cells and the Regeneration of the Aging Cardiovascular System

Mechanisms of Cardiovascular Disease in Accelerated Aging Syndromes

Mechanisms Underlying Caloric Restriction, Lipid Metabolism, and Life Span Regulation
Issei Komuro Guest Editor

In the past several years, remarkable progress has been made in the understanding of the mechanisms of premature aging. These rare, genetic conditions offer valuable insights into the normal aging process and the complex biology of cardiovascular disease. Many of these advances have been made in the most dramatic of these disorders, Hutchinson–Gilford progeria syndrome. Although characterized by features of normal aging such as alopecia, skin wrinkling, and osteoporosis, patients with Hutchinson–Gilford progeria syndrome are affected by accelerated, premature arteriosclerotic disease that leads to heart attacks and strokes at a mean age of 13 years. In this review, we highlight recent advances in the biology of premature aging uncovered in Hutchinson–Gilford progeria syndrome and other accelerated aging syndromes, advances that provide insight into the mechanisms of cardiovascular diseases ranging from atherosclerosis to arrhythmias.

Key Words: premature aging • progeria • Werner syndrome • genome instability

This article has been cited by other articles:

				B. C. Capell, M. Olive, M. R. Erdos, K. Cao, D. A. Faddah, U. L. Tavarez, K. N. Conneely, X. Qu, H. San, S. K. Ganesh, et al. A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model PNAS, October 14, 2008; 105(41): 15902 - 15907. [Abstract] [Full Text] [PDF]