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(Circulation Research. 2001;88:858.)
© 2001 American Heart Association, Inc.

Editorial

Angiotensin II–Stimulated Vascular Remodeling

The Search for the Culprit Oxidase

Kaikobad Irani

From the Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md.

Correspondence to Kaikobad Irani, Ross 1023, The Johns Hopkins University School of Medicine, 720 Rutland Ave, Baltimore, MD 21205. E-mail kirani@jhmi.edu

Key Words: NAD(P)H oxidase • angiotensin II • smooth muscle • medial hypertrophy • reactive oxygen species

	Introduction

 
Hypertrophy and hyperplasia of vascular smooth muscle cells are hallmarks of the common vascular disorders of atherosclerosis, restenosis, and hypertension and contribute to their long-term sequelae. Angiotensin II (Ang II) is a potent smooth muscle mitogen and hypertrophic agent. The importance of Ang II in the pathogenesis of vascular disease is reflected in the efficacy of angiotensin-converting enzyme inhibitors and Ang II receptor blockers in the treatment of atherosclerosis and hypertension. Despite the widespread use of these agents in clinical practice, our understanding of the mechanisms through which Ang II exerts its effects on the vasculature is not complete. The studies by Lassègue et al¹ and Wang et al² in this issue of Circulation Research go a long way in elucidating the molecular basis for the effects of Ang II on vascular smooth muscle cell growth.

To fully appreciate the significance of the reported findings, one has to place them into historical perspective. The role of oxidative stress in the pathogenesis of the above-mentioned vascular disorders has been well recognized for some time.³ It has come to light that humoral factors, such as Ang II, platelet-derived growth factor, and thrombin, directly lead to oxidative stress in smooth muscle cells via the generation of reactive oxygen species (ROS), which are essential for their mitogenic and hypertrophic properties.^{4 5 6 7} With these findings in hand, investigators directed their efforts toward identifying the enzymatic source of growth factor–stimulated ROS in vascular smooth muscle cells.

Attention was mainly focused on identifying an oxidase functionally analogous to . . . [Full Text of this Article]

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