This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Potente, M. Articles by Dimmeler, S. Search for Related Content PubMed Articles by Potente, M. Articles by Dimmeler, S. Related Collections Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1577.)
© 2008 American Heart Association, Inc.

Editorials

NO Targets SIRT1

A Novel Signaling Network in Endothelial Senescence

Michael Potente; Stefanie Dimmeler

From the Institute for Cardiovascular Regeneration (M.P., S.D.), Centre of Molecular Medicine, and the Department of Cardiology (M.P.), Internal Medicine III, Goethe University, Frankfurt, Germany.

Correspondence to Stefanie Dimmeler, PhD, Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, D-60590 Frankfurt (Main), Germany. E-mail dimmeler@em.uni-frankfurt.de

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

	Introduction

 
Aging is considered to be a major risk factor for the development of cardiovascular diseases, the leading cause of morbidity and mortality in Western countries. Among the age-associated functional and structural changes in the vascular wall, particularly endothelial function declines during the ageing process. Impairment of endothelial function critically contributes to the pathogenesis of several cardiovascular diseases (eg, atherosclerosis) and is manifested in its earliest form as an attenuation of endothelium-dependent dilator responses as a consequence of an alteration in the expression or activity of the endothelial nitric oxide (NO) synthase (eNOS) and increased oxidative stress. Endothelial senescence appears to play a key role in the process of vascular aging, affecting vascular tone, blood vessel growth, and regeneration. Thus, identifying new molecular targets involved in senescence signaling offers opportunities to potentially improve endothelial cell function and cardiovascular disease progression.

See accompanying article on page 1634

In a study published in the present issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Ota et al report that the PDE3 inhibitor cilostazol prevents endothelial premature senescence by a NO-dependent upregulation of SIRT1, a key regulator of ageing and longevity in lower organisms.¹ Apart from the relevance of these findings for improving the understanding of vascular endothelial senescence pathways, they point to SIRT1 as an important modulator of signaling networks critical for maintaining vascular endothelial homeostasis and suggest novel therapeutic opportunities for the treatment of cardiovascular diseases.

	Sirtuins, Senescence, and Aging

 
Cellular senescence has been used as a model for mammalian aging. This process consists of a state . . . [Full Text of this Article]

Related Article:

Cilostazol Inhibits Oxidative Stress–Induced Premature Senescence Via Upregulation of Sirt1 in Human Endothelial Cells

Hidetaka Ota, Masato Eto, Mitsunobu R. Kano, Sumito Ogawa, Katsuya Iijima, Masahiro Akishita, and Yasuyoshi Ouchi
Arterioscler Thromb Vasc Biol 2008 28: 1634-1639. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				A. Farsetti, A. Grasselli, S. Bacchetti, C. Gaetano, and M. C. Capogrossi The telomerase tale in vascular aging: regulation by estrogens and nitric oxide signaling J Appl Physiol, January 1, 2009; 106(1): 333 - 337. [Abstract] [Full Text] [PDF]