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Monocyte chemoattractant protein-1 and atherosclerosis: is there room for an additional biomarker?
Blai Coll1, Carlos Alonso-Villaverde, Jorge Joven
1Centre de Recerca Biomedica, Hospital Universitari Sant Joan, 43201, Reus, Spain.
Insights
Monocyte chemoattractant protein-1 (CCL2) drives atherosclerosis by recruiting inflammatory cells. While CCL2/CCR2 targeting shows promise, its role as a diagnostic biomarker in humans requires further investigation due to conflicting results.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Atherosclerosis is an inflammatory disease involving chemokines.
- Monocyte chemoattractant protein-1 (CCL2) and its receptor CCR2 are key players in inflammatory cell recruitment.
- The CCL2/CCR2 pathway's role in atherosclerosis is well-established in animal models.
Purpose of the Study:
- To review the implicated role of CCL2 in atherosclerosis.
- To evaluate the potential of the CCL2/CCR2 pathway as a diagnostic, prognostic, and therapeutic target.
- To address the controversies surrounding CCL2 as a human biomarker.
Main Methods:
- Review of animal studies on CCL2 and CCR2 gene/receptor manipulation.
- Analysis of human studies correlating plasma CCL2 levels with atherosclerosis.
- Assessment of the limitations of current analytical tools for biomarker validation.
Main Results:
- Genetic manipulation of CCL2/CCR2 significantly impacts atherosclerosis development in animals.
- Human studies show a link between plasma CCL2 and atherosclerosis, but it's often confounded by classical risk factors.
- Current analytical methods lack the robustness for definitive conclusions on CCL2 as a biomarker.
Conclusions:
- The CCL2/CCR2 pathway is a critical component of atherosclerosis pathogenesis.
- Further research is needed to validate CCL2/CCR2 as a reliable biomarker for atherosclerosis.
- The pathway holds potential for future diagnostic, prognostic, and therapeutic strategies in cardiovascular disease.
Abstract:
Atherosclerosis is an inflammatory disease in which several chemokines are implicated. The roles of these molecules extend from the recruitment of circulating inflammatory cells to the activation of inflammatory and pro-thrombotic cascades, which ultimately leads to an atherosclerosis-related event. One of the most studied chemokines is monocyte chemoattractant protein-1 (CCL2), which has been strongly linked to atherosclerosis in both animal and human studies. The higher the expression of either the CCL2 gene or its receptor CCR-2, the higher the likelihood of developing atherosclerosis in genetically-modified animals. Conversely, the deletion of either CCL2 or its receptor is followed by a significant reduction in the development of atherosclerotic plaques. Studies in humans yield controversial results. Most of these studies linked the plasma CCL2 concentration to the occurrence of atherosclerosis or related events; however, this relationship does not seem to be independent of the classical, known risk factors. Currently, there are no suitable analytical tools to reach strong conclusions with respect to the value of plasma CCL2 concentration as a biomarker of atherosclerosis, but experimental evidence suggests that the CCL2/CCR2 pathway should be further explored as a diagnostic, prognostic and therapeutic target.
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