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Updated: Jul 31, 2026

On-Chip Endothelial Inflammatory Phenotyping
Published on: July 22, 2012
Modulation of atherogenesis by chemokines
1Department of Medicine, Vascular Medicine Research, Brigham and Women's Hospital, Harvard Medical School, 65 Lansdowne Street, Rm. 286, Cambridge, MA 02139, USA. wboisvert@rics.bwh.harvard.edu
Abstract:
Migration of leukocytes into the vasculature-which involves the concerted effort of many molecules, including chemokines-is a requisite step for atherogenesis. The three chemokines that have been implicated most strongly in atherogenesis are monocyte chemoattractant protein 1 (MCP-1), interleukin 8 (IL-8)/growth-regulated oncogene alpha (Gro-alpha), and fractalkine. Although all three chemokines appear to impact atherogenesis by attenuating monocyte/macrophage accumulation in the lesion, the precise mechanism of action of each of the chemokines, as well as their interactive role in atherosclerosis, have not been elucidated. This review focuses on the latest findings that describe the individual roles of MCP-1, IL-8/Gro-alpha, and fractalkine on macrophage recruitment in atherosclerosis. Furthermore, based on present knowledge of the participation of these three chemokines and their receptors in monocyte/macrophage recruitment, a possible interactive role of these chemokines in atherogenesis is explored.
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