This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sedding, D. Articles by Haendeler, J. Search for Related Content PubMed PubMed Citation Articles by Sedding, D. Articles by Haendeler, J. Related Collections Related Article

(Circulation Research. 2007;100:1396.)
© 2007 American Heart Association, Inc.

Editorials

Do We Age on Sirt1 Expression?

Daniel Sedding, Judith Haendeler

From the Department of Cardiology, University of Giessen (D.S.), Germany; IUF at the University of Duesseldorf (J.H.), Germany.

Correspondence to Judith Haendeler, PhD, Molecular Cell & Aging Research, IUF at the University of Duesseldorf gGmbH, Auf‘m Hennekamp 50, 40225 Duesseldorf, Germany. E-mail juhae001@uni-duesseldorf.de

See related article, pages 1512–1521

Key Words: sirtuins • aging • cardiac hypertrophy • oxidative stress

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

Aging leads to a progressive decline in multiple organ systems, including the heart. Heart failure in response to cellular aging and chronic or acute cellular stresses represents one of the major burdens of the western civilization. Over the last 15 years, the interest in the therapeutic use of caloric restriction to prevent aging has emerged. However, it is difficult to determine whether caloric restriction influences longevity in humans because no validated biomarker exists, which can serve as a surrogate marker of aging and it is impossible to conduct a randomized, diet-controlled long-term survival study in humans. Nevertheless, caloric restriction has been shown in several studies to lower fasting plasma glucose concentration and serum low-density lipoprotein cholesterol, to decrease insulin resistance, visceral fat mass and the levels of inflammatory markers. Most of these markers are known to be risk factors for coronary heart disease. Thus, even it is not known whether caloric restriction does prolong maximum life-span, it could increase life expectancy and the quality of late life by reducing the burden of chronic diseases. However, the precise biological and cellular mechanisms responsible for aging and the antiaging effects of caloric restriction are not known. Moreover, even if caloric restriction would result in an increase in maximum life span in humans, it will be difficult to maintain long-term caloric restriction in modern society. Therefore, one major interest is to develop caloric restriction mimetics to provide all of the "healthy" physiological, metabolic and hormonal effects of caloric restriction without the need to . . . [Full Text of this Article]

Related Article:

Sirt1 Regulates Aging and Resistance to Oxidative Stress in the Heart

Ralph R. Alcendor, Shumin Gao, Peiyong Zhai, Daniela Zablocki, Eric Holle, Xianzhong Yu, Bin Tian, Thomas Wagner, Stephen F. Vatner, and Junichi Sadoshima
Circ. Res. 2007 100: 1512-1521. [Abstract] [Full Text] [PDF]