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Papers In Press, published online ahead of print June 16, 2005
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Medicine 0682, BSB 1080, University of California, San Diego, La Jolla, CA 92093
Corresponding Author: 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 over 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.
Revised on June 9, 2005
Accepted on June 9, 2005
Molecular mechanisms regulating monocyte recruitment in atherosclerosis
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