HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yang, Z. Articles by Ming, X.-F. Search for Related Content PubMed PubMed Citation Articles by Yang, Z. Articles by Ming, X.-F.

Recent Advances in Understanding Endothelial Dysfunction in Atherosclerosis

Zhihong Yang, MD, Department of Medicine, Division of Physiology, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland
Xiu-Fen Ming, MD, PhD, Department of Medicine, Division of Physiology, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland

Reprint Requests: Prof. Zhihong Yang, MD, Vascular Biology Laboratory, Department of Medicine, Division of Physiology, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland, Tel: 41-26-300 85 93; Fax: 41-26-300 96 36; Email: zhihong.yang{at}unifr.ch

Over the last two decades, it has become evident that decreased bioavailability of endothelial nitric oxide (NO) produced from endothelial NO synthase (eNOS), referred to as endothelial dysfunction, plays a crucial role in the development and progression of atherosclerosis. Much progress has been made in understanding the mechanisms of decreased endothelial NO bioavailability at the levels of regulation of eNOS gene expression, eNOS enzymatic activity and NO inactivation. Initial studies suggest that increasing eNOS gene expression would improve endothelial NO release in the hope of inhibiting the progression of atherosclerosis. Recent experimental studies, however, do not always support this therapeutic concept and show some evidence that overexpression of eNOS in atherosclerosis may be even harmful for the disease progression.Thus, recent research to improve endothelial function in atherosclerosis has focused on regulation of eNOS enzymatic activity and prevention of NO inactivation by oxidative stress. Since the role of oxidative stress in endothelial NO bioavailability has been reviewed in a large number of comprehensive articles, this article focuses on the relevant regulatory mechanisms of eNOS enzymatic activity that are emerging to play a role in endothelial dysfunction in atherosclerosis.

Key Words: Arginase • Atherosclerosis • BH₄ • eNOS • L-arginine • Oxidative stress

This article has been cited by other articles:

				G. Spinetti, N. Kraenkel, C. Emanueli, and P. Madeddu Diabetes and vessel wall remodelling: from mechanistic insights to regenerative therapies Cardiovasc Res, May 1, 2008; 78(2): 265 - 273. [Abstract] [Full Text] [PDF]

				A. J. Webb, N. Patel, S. Loukogeorgakis, M. Okorie, Z. Aboud, S. Misra, R. Rashid, P. Miall, J. Deanfield, N. Benjamin, et al. Acute Blood Pressure Lowering, Vasoprotective, and Antiplatelet Properties of Dietary Nitrate via Bioconversion to Nitrite Hypertension, March 1, 2008; 51(3): 784 - 790. [Abstract] [Full Text] [PDF]

				A. Vinh, R. E. Widdop, G. R. Drummond, and T. A. Gaspari Chronic angiotensin IV treatment reverses endothelial dysfunction in ApoE-deficient mice Cardiovasc Res, January 1, 2008; 77(1): 178 - 187. [Abstract] [Full Text] [PDF]

				H. Viswambharan, J. M. Carvas, V. Antic, A. Marecic, C. Jud, C. E. Zaugg, X.-F. Ming, J.-P. Montani, U. Albrecht, and Z. Yang Mutation of the Circadian Clock Gene Per2 Alters Vascular Endothelial Function Circulation, April 24, 2007; 115(16): 2188 - 2195. [Abstract] [Full Text] [PDF]