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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1928-1936
Published online before print August 28, 2008, doi: 10.1161/ATVBAHA.108.162925
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1928.)
© 2008 American Heart Association, Inc.


Brief Reviews

Chemokines as Mediators of Neovascularization

Ellen C. Keeley; Borna Mehrad; Robert M. Strieter

From the Department of Medicine, Divisions of Cardiology (E.C.K.) and Pulmonary and Critical Care Medicine (B.M., R.M.S.), University of Virginia, Charlottesville.

Correspondence to Robert M. Strieter, MD, University of Virginia, Department of Medicine, Division of Pulmonary Critical Care, Box 800466, Charlottesville, VA 22908-0466. E-mail Strieter{at}Virginia.edu

Series Editor: Christian Weber
ATVB In Focus

Chemokines in Atherosclerosis, Thrombosis, and Vascular Biology

Chemokines are a superfamily of homologous heparin-binding proteins, first described for their role in recruiting leukocytes to sites of inflammation. Chemokines have since been recognized as key factors mediating both physiological and pathological neovascularization in such diverse clinical settings as malignancy, wound repair, chronic fibroproliferative disorders, myocardial ischemia, and atherosclerosis. Members of the CXC chemokine family, structurally defined as containing the ELR amino acid motif, are potent inducers of angiogenesis, whereas another subset of the CXC chemokines inhibits angiogenesis. In addition, CCL2, a CC chemokine ligand, has been implicated in arteriogenesis. In this article, we review the current literature on the role of chemokines as mediators of neovascularization.


Key Words: angiogenesis • cytokines • arteriogenesis • chemokines