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(Circulation Research. 2004;94:703.)
© 2004 American Heart Association, Inc.

Editorials

Younger Than Yesterday

Is Vascular Senescence a Two-Way Street?

Cam Patterson, Marschall S. Runge, Nageswara Madamanchi

From the Carolina Cardiovascular Biology Center and Department of Medicine (C.P., M.S.R., N.M.); Departments of Pharmacology and Cell and Developmental Biology (C.P.), University of North Carolina, Chapel Hill, NC.

Correspondence to Cam Patterson, MD, Director, Carolina Cardiovascular Biology Center, University of North Carolina at Chapel Hill, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599-7126. E-mail cpatters@med.unc.edu

Key Words: endothelium • oxidative stress • aging • telomerase

An extract of the first 250 words of the full text is provided, because this article has no abstract.

A therosclerotic cardiovascular disease is an intrinsically age-related process, and epidemiologic data support the idea that the milieu of the elderly body, rather than a diseased blood vessel’s age, determines this susceptibility to atherosclerosis and its consequences. This notion, if true, suggests that vascular senescence may be a reversible process and raises the possibility of rejuvenative therapies for cardiovascular protection in the elderly. A report by Haendeler and colleagues in this issue of Circulation Research¹ addresses the mechanisms by which cultured vascular endothelial cells undergo senescence and suggests that both antioxidant mechanisms and statins, the pharmacologic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, may reverse at least some features of the vascular senescence phenotype. What can we learn about vascular aging from this impressive report?

Do Aging and Replicative Senescence Go Hand in Hand?

The title of this article indicates that the authors are interested in replicative senescence of endothelial cells in cell culture as a model for understanding the mechanisms that underlie vascular aging. In now classic experiments, Leonard Hayflick discovered that somatic cells in culture cannot divide indefinitely.² Replicative senescence therefore refers to the process by which cells lose their ability to replicate after a finite number of cell divisions, and Hayflick (among many others) noted that somatic cells exhausted of their ability to divide in culture may have characteristics associated with aging. This led to the notion that replicative senescence might account for organismal aging in vivo and, conversely, that the phenomenon of replicative senescence in culture might be a practical model for understanding the mechanisms . . . [Full Text of this Article]

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