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Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2292-2301
Published online before print August 2, 2007, doi: 10.1161/ATVBAHA.107.149179
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Right arrow Vascular Adhesion Molecules
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2292.)
© 2007 American Heart Association, Inc.


Brief Reviews

Vascular Adhesion Molecules in Atherosclerosis

Elena Galkina; Klaus Ley

From the Department of Biomedical Engineering and Robert M. Berne Cardiovascular Research Center, University of Virginia, Health Sciences Center, Charlottesville, Va.

Correspondence to Klaus Ley, Robert M. Berne Cardiovascular Research Center, University of Virginia, P.O. Box 801394, Charlottesville, VA 22908. E-mail klausley{at}virginia.edu

Series Editor: Dietmar Vestweber Previous Brief Reviews in this Series:

•van Buul JD, Kanters E, and Hordijk PL. Endothelial signaling by Ig-like cell adhesion molecules. Atheroscler Thromb Vasc Biol. 2007;27:1870–1876.
•Bradfield PF, Nourshargh S, Aurrand-Lions M, Imhof BA. JAM family and related proteins in leukocyte migration. Atheroscler Thromb Vasc Biol. 2007;27:2104–2112.

Numerous reports document the role of vascular adhesion molecules in the development and progression of atherosclerosis. Recent novel findings in the field of adhesion molecules require an updated summary of current research. In this review, we highlight the role of vascular adhesion molecules including selectins, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule1 (ICAM-1), PECAM-1, JAMs, and connexins in atherosclerosis. The immune system is important in atherosclerosis, and significant efforts are under way to understand the vascular adhesion molecule–dependent mechanisms of immune cell trafficking into healthy and atherosclerosis-prone arterial walls. This review focuses on the role of vascular adhesion molecules in the regulation of immune cell homing during atherosclerosis and discusses future directions that will lead to better understanding of this disease.

Leukocyte and endothelial adhesion molecules play key roles in the development and progression of atherosclerosis. In animal models, blocking or eliminating P-selectin, VCAM-1 or {alpha}4β1 integrin reduces atherosclerotic lesion formation by more than 50%. Smaller effects are seen by manipulating E-selectin, ICAM-1 or the JAM family of adhesion molecules.


Key Words: atherosclerosis • pathophysiology • lymphocyte • leukocyte • monocyte • macrophages • trafficking




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