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Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Chemokines and atherosclerosis
Yuri Sheikine1, Göran K Hansson
1Center for Molecular Medicine, Cardiovascular Research Unit, Karolinska Institute, Stockholm, Sweden. yuri.sheikine@cmm.ki.se
Insights
Chemokines, crucial for inflammation, drive leukocyte accumulation in atherosclerosis. Targeting these signaling pathways offers a promising strategy for anti-atherogenic therapies.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Atherosclerosis is an inflammatory disease involving leukocyte accumulation in vessel walls.
- Chemokines are polypeptides that attract cells to inflammatory sites via G-protein coupled receptors.
- These molecules play critical roles in various physiological and pathological conditions, including atherosclerosis.
Purpose of the Study:
- To explore the role of chemokines in the development and progression of atherosclerosis.
- To identify specific chemokines involved in leukocyte trafficking and retention within atherosclerotic plaques.
- To assess the potential of chemokines and their receptors as clinical markers and therapeutic targets for atherosclerosis.
Main Methods:
- Review of in vivo and in vitro investigations on chemokine function in inflammation.
- Analysis of studies examining the expression and function of specific chemokines (e.g., MCP-1, RANTES, CXCL16) in atherosclerosis.
- Examination of research on viral chemokine homologues and their potential role in pathogenesis.
Main Results:
- Chemokines like MCP-1, MCP-4, MIP-1, and RANTES mediate leukocyte recruitment and retention in atherosclerotic plaques.
- CXCL16 exhibits a dual role as both a chemokine and a scavenger receptor.
- Viral chemokine homologues may contribute to atherosclerosis pathogenesis.
- Chemokine expression levels and gene polymorphisms show potential as clinical markers for cardiovascular diseases.
Conclusions:
- Chemokines are key mediators of leukocyte trafficking in atherosclerosis.
- Targeting chemokine signaling pathways presents a viable anti-atherogenic therapeutic strategy.
- Chemokines and their receptors hold promise as biomarkers for cardiovascular disease risk and progression.
Abstract:
Atherosclerosis is an inflammatory disease of the vessel wall, characterized by the accumulation of leukocytes, especially macrophages and T-cells. Chemokines are small heparin-binding polypeptides, whose main function is to attract cells to the areas of developing inflammation. They function by ligating G-protein coupled chemokine receptors initiating different signaling cascades. In vivo and in vitro investigations showed that chemokines are produced by a variety of cells and play important roles in the development and progression of many physiological and pathological conditions including atherosclerosis. Chemokines such as MCP-1, MCP-4, MIP-1 and RANTES may mediate leukocyte trafficking to, and their retention in, the plaque while CXCL16 seems to fulfill the dual function of a chemokine and a scavenger receptor. Chemokine and chemokine receptor homologues are secreted by several viruses, which may also play a role in the pathogenesis of atherosclerosis. Expression levels and gene polymorphisms of some chemokines may become useful clinical markers of atherosclerosis and other cardiovascular diseases. Modulation of chemokines and chemokine receptors' expression as well as their signaling pathways may provide important anti-atherogenic strategies.
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