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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:461.)
© 2007 American Heart Association, Inc.

ATVB In Focus

Role of Oxidative Stress in the Pathogenesis of Abdominal Aortic Aneurysms

Michael L. McCormick; Dan Gavrila; Neal L. Weintraub

From the Department of Internal Medicine (M.L.M., D.G.) and Department of Radiation Oncology (M.L.M.), University of Iowa Carver College of Medicine, Iowa City; the Department of Internal Medicine, Cardiovascular Division (N.L.W.), University of Cincinnati College of Medicine, Ohio; and Research Service, Veteran’s Administration Medical Center (N.L.W.), Cincinnati, Ohio.

Correspondence to Dr Neal L. Weintraub, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Cincinnati College of Medicine, 231 Albert Sabin Way, ML 0542, MSB 3363, PO Box 670542, Cincinnati, OH 45267-0542. E-mail neal.weintraub{at}uc.edu

Series Editor: Robert W. Thompson Previous Brief Reviews in this Series:

•Powell JT, Brady AR. Detection, management, and prospects for the medical treatment of small abdominal aortic aneurysms. 2004;24:241–245.
•Daugherty A, Cassis LA. Mouse models of abdominal aortic aneurysms. 2004;24:429–434.
•Pasterkamp G, Galis ZS, de Kleijn DPV. Expansive arterial remodeling: location, location, location. 2004;24:650–657.
•Vorp DA, Vande Geest JP. Biomechanical determinants of abdominal aortic aneurysm rupture. 2005;25:1558–1566.
•Shimizu K, Mitchell RN, Libby P. Inflammation and cellular immune response in abdominal aortic aneurysms. 2006;26:987–994.

The role of inflammation in the pathogenesis of abdominal aortic aneurysms (AAA) is well established. The inflammatory process leads to protease-mediated degradation of the extracellular matrix and apoptosis of smooth muscle cells (SMC), which are the predominant matrix synthesizing cells of the vascular wall. These processes act in concert to progressively weaken the aortic wall, resulting in dilatation and aneurysm formation. Oxidative stress is invariably increased in, and contributes importantly to, the pathophysiology of inflammation. Moreover, reactive oxygen species (ROS) play a key role in regulation of matrix metalloproteinases and induction of SMC apoptosis. ROS may also contribute to the pathogenesis of hypertension, a risk factor for AAA. Emerging evidence suggests that ROS and reactive nitrogen species (RNS) are associated with AAA formation in animal models and in humans. Although experimental data are limited, several studies suggest that modulation of ROS production or activity may suppress AAA formation and improve experimental outcome in rodent models. Although a number of enzymes can produce injurious ROS in the vasculature, increasing evidence points toward a role for NADPH oxidase as a source of oxidative stress in the pathogenesis of AAA.

Key Words: aneurysm • reactive oxygen species • oxidative stress • NADPH oxidase • inflammation

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