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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:1412.)
© 2009 American Heart Association, Inc.

Brief Reviews

Regulation of the Migration and Survival of Monocyte Subsets by Chemokine Receptors and Its Relevance to Atherosclerosis

Emmanuel L. Gautier; Claudia Jakubzick; Gwendalyn J. Randolph

From the Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York.

Correspondence to Gwendalyn J. Randolph, PhD, Department of Gene and Cell Medicine, 1425 Madison Avenue, Box 1496, New York, NY 10029. E-mail Gwendalyn.randolph{at}mssm.edu

Series Editor: Ziad Mallat
ATVB In Focus

Monocyte Subsets and Their Relevance to Cardiovascular Diseases

Monocytes are central mediators in the advance of atherosclerotic plaque, making them a natural therapeutic target for reducing disease burden. Here, we highlight recent advances in our current understanding of monocyte heterogeneity and its relevance to regulation of monocyte accumulation and function within atherosclerotic plaques. Differences that distinguish monocyte subsets include differential expression of chemokine receptors, especially CCR2 and CX3CR1. Ablation of expression of these 2 receptors (or their ligands) in mice has an additive inhibition on monocyte recruitment to atherosclerotic plaques. Moreover, simultaneously interfering with 3 key pathways—CCR2, CX3CR1, and CCR5—essentially abolishes atherosclerosis in mice. Here, we discuss how these chemokine receptors act at multiple points on at least 1 monocyte subset, regulating their mobilization from bone marrow, survival, or recruitment to plaques. Finally, we discuss how this knowledge may be useful clinically, emphasizing that CX3CR1 may in particular be a viable target for therapeutic manipulation of monocyte-derived cell fate in cardiovascular disease.

Key Words: chronic inflammation • arteriosclerosis • macrophage • chemotaxis • diapedesis