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Journal of Lipid Research, Vol. 46, 1582-1590, August 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Thematic Review

Thematic Review Series: The Immune System and Atherogenesis. Molecular mechanisms regulating monocyte recruitment in atherosclerosis

Oswald Quehenberger¹

Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0682

Published, JLR Papers in Press, June 16, 2005. DOI 10.1194/jlr.R500008-JLR200

¹ To whom correspondence should be addressed. e-mail: oquehenberger{at}ucsd.edu

Cardiovascular disease, a progressive disorder characterized by the accumulation of lipids in the artery wall, is a leading cause of death in Western societies. One of the initial events in atherogenesis involves the recruitment of inflammatory cells from the circulation into the developing lesion. Studies during the past decade have underscored the role of inflammatory mediators in disease initiation and progression. Critical progress has been made in our understanding of the complex mechanisms by which monocytes, macrophages, and T-cells accumulate in atherosclerotic plaques. Experimental research has identified several candidate adhesion proteins and chemokines that are critically involved in the recruitment process, and encouraging data provide a mechanistic framework for new therapeutic targets.

This review provides an overview of our current understanding of the mechanisms that direct the recruitment of monocytes to, and their retention in, atherosclerotic lesions.

Abbreviations: apoE^–/–, apolipoprotein E-deficient; CX3CL1, fractalkine; CX3CR1, receptor for fractalkine; EC, endothelial cell; GRO, growth-related oncogene; ICAM-1, intracellular adhesion molecule-1; IL-8, interleukin-8; KC, keratinocyte chemokine; LDLR^–/–, low density lipoprotein receptor-deficient; MCP-1, monocyte chemoattractant protein-1; MIP, macrophage inflammatory protein; RANTES, regulated on activation normal T-cell expressed and secreted; SMC, smooth muscle cell; SR-A, scavenger receptor A; VCAM-1, vascular cell adhesion molecule-1

Supplementary key words adhesion molecules • cardiovascular disease • chemokines • inflammation • leukocytes • receptors

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