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Updated: Nov 23, 2025

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Published on: April 3, 2017
Role of Macrophages and RhoA Pathway in Atherosclerosis
Malgorzata Kloc1,2,3, Ahmed Uosef1,2, Jacek Z Kubiak4,5
1Houston Methodist Research Institute, Houston, TX 77030, USA.
Abstract:
The development, progression, or stabilization of the atherosclerotic plaque depends on the pro-inflammatory and anti-inflammatory macrophages. The influx of the macrophages and the regulation of macrophage phenotype, inflammatory or anti-inflammatory, are controlled by the small GTPase RhoA and its downstream effectors. Therefore, macrophages and the components of the RhoA pathway are attractive targets for anti-atherosclerotic therapies, which would inhibit macrophage influx and inflammatory phenotype, maintain an anti-inflammatory environment, and promote tissue remodeling and repair. Here, we discuss the recent findings on the role of macrophages and RhoA pathway in the atherosclerotic plaque formation and resolution and the novel therapeutic approaches.
Insights
Macrophages and the RhoA pathway are key to atherosclerotic plaque development and resolution. Targeting these components offers a promising therapeutic strategy for atherosclerosis, promoting repair and reducing inflammation.
Area of Science:
- Cardiovascular Biology
- Cell Signaling
- Immunology
Background:
- Atherosclerotic plaque stability, progression, and development are influenced by macrophage polarization.
- Macrophage recruitment and phenotype are regulated by the small GTPase RhoA and its effectors.
Purpose of the Study:
- To review the roles of macrophages and the RhoA pathway in atherosclerosis.
- To discuss novel therapeutic strategies targeting these pathways.
Main Methods:
- Literature review of recent findings on macrophages and RhoA in atherosclerosis.
- Analysis of therapeutic approaches targeting macrophage influx and phenotype.
Main Results:
- Macrophages are crucial in both the formation and resolution phases of atherosclerotic plaques.
- The RhoA pathway significantly controls macrophage behavior within atherosclerotic lesions.
Conclusions:
- Targeting macrophages and the RhoA pathway presents a viable therapeutic avenue for anti-atherosclerotic treatments.
- Inhibiting macrophage influx and inflammatory phenotypes, while promoting repair, is a key therapeutic goal.
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