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on September 25, 2008

Arteriosclerosis, Thrombosis, and Vascular Biology. 2008
Published online before print September 25, 2008, doi: 10.1161/ATVBAHA.107.161224
A more recent version of this article appeared on November 1, 2008
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Submitted on May 12, 2008
Accepted on September 15, 2008

Chemokines in Vascular Dysfunction and Remodeling

Andreas Schober *

From the Cardiology Unit, Medical Policlinic-City Center Campus, University of Munich, Germany.

* To whom correspondence should be addressed. E-mail: andreas.schober{at}med.uni-muenchen.de.

Abstract—Vascular remodeling stands for structural changes of the vessel wall in response to various noxious stimuli, which results in reorganization of the vessel wall architecture. Luminal narrowing because of neointima formation and constrictive remodeling leading to hypoperfusion is the most relevant clinical effect. Smooth muscle cell (SMC) accumulation, inflammatory cell recruitment, and endothelial regeneration are the critical parts in obstructive vascular remodeling. Chemokines and chemokine receptors have a great impact on initiating and progressing neointimal formation by controlling each step of the remodeling process. SDF-1{alpha} regulates vascular repair by CXCR4-dependent smooth muscle progenitor cell recruitment, which contributes to the maladaptive response to injury. The three distinct chemokine-chemokine receptor pairs MCP-1/CCR2, RANTES/CCR5, and Fractalkine/CX3CR1 direct lesional leukocyte infiltration. In addition MCP-1/CCR2 and Fractalkine/CX3CR1 increase neointimal SMC expansion. In contrast, KC/Gro-{alpha} supports endothelial recovery through CXCR2, which attenuates neointima formation. These findings highlight the importance to characterize specific functions of the chemokine network to enable therapeutic intervention.




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