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Published Online
on August 28, 2008

Arteriosclerosis, Thrombosis, and Vascular Biology. 2008
Published online before print August 28, 2008, doi: 10.1161/ATVBAHA.108.162925
A more recent version of this article appeared on November 1, 2008
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Submitted on July 31, 2008
Accepted on August 18, 2008

Chemokines as Mediators of Neovascularization

Ellen C. Keeley ; Borna Mehrad ; and 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.

* To whom correspondence should be addressed. E-mail: Strieter{at}Virginia.edu.

Abstract—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