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Updated: Jul 15, 2026

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
The specific role of chemokines in atherosclerosis
Vincent Braunersreuther1, François Mach, Sabine Steffens
1Division of Cardiology, Department of Medicine, Geneva University Hospital, Foundation for Medical Researches, 64 Avenue Roseraie, 1211 Geneva, Switzerland.
Insights
Blocking chemokine and chemokine receptor interactions may treat atherosclerosis and related heart conditions. Targeting leukocyte recruitment offers potential therapeutic strategies for inflammatory diseases like myocardial infarction.
Area of Science:
- Cardiovascular Science
- Immunology
- Inflammation Biology
Background:
- Atherosclerosis is a chronic inflammatory condition causing heart disease and stroke.
- Inflammatory cell recruitment to the intima is crucial for atherosclerosis development.
- Chemokines and their receptors mediate this inflammatory cell recruitment.
Purpose of the Study:
- To explore the role of chemokines in atherosclerosis.
- To investigate the potential of targeting chemokine pathways for therapeutic intervention.
Main Methods:
- Review of existing literature on chemokine involvement in atherosclerosis.
- Analysis of findings from animal models investigating chemokine antagonists.
Main Results:
- Several CC and CXC chemokine families, including MCP-1/CCL2, IL-8/CCL8, IP-10/CXCL10, SDF-1/CXCL12, and fractalkine/CX3CL1, are implicated in atherosclerosis.
- Animal models suggest blocking chemokine/chemokine receptor interactions can impede atherosclerosis progression.
Conclusions:
- Chemokine pathways are critical in the inflammatory processes underlying atherosclerosis.
- Inhibiting chemokine-mediated leukocyte recruitment presents a promising therapeutic avenue for atherosclerosis and myocardial infarction treatment.
Abstract:
Atherosclerosis is a chronic inflammatory disease that represents the primary cause of heart disease and stroke. The recruitment of inflammatory cells in the intima is an essential step in the development and progression of atherosclerosis. This process is triggered by local production of chemokines and chemokine receptors from activated endothelial cells and inflammatory cells. Various members of the CC chemokine family (e.g. MCP-1/CCL2) as well as CXC family (e.g. IL-8/CCL8, IP-10/CXCL10, SDF-1/CXCL12) and, more recently, fractalkine/CX3CL1 have been implicated in atherosclerosis development. Latest findings in animal models suggest that blocking chemokine/chemokine receptor interactions may serve as a suitable approach to treat atherosclerosis. Likewise, chemokine antagonists that inhibit leukocyte recruitment could particularly be interesting to treat inflammation in response to myocardial infarction, the major consequence of atherosclerosis.
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