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Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Targeting Macrophages in Atherosclerosis
Dan Hu1, Zengyan Wang2, Yuzhong Wang3
1Department of Cardiovasology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, China.
Insights
Macrophages are key inflammatory cells in atherosclerosis (AS), a major cause of cardiovascular disease. Understanding how these cells drive AS progression or regression offers new therapeutic targets.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathology
Background:
- Atherosclerosis (AS) is a chronic inflammatory disease underlying Coronary Atherosclerotic Disease (CAD) and stroke.
- Macrophages are central inflammatory cells in atherosclerotic lesions, critically influencing plaque development and regression.
- Both pro-inflammatory and anti-inflammatory factors modulate macrophage behavior in AS.
Purpose of the Study:
- To review the multifaceted roles of macrophages in the pathogenesis of atherosclerosis.
- To elucidate the regulatory mechanisms by which macrophages influence AS development and progression.
- To highlight macrophages as potential therapeutic targets for AS diagnosis and treatment.
Main Methods:
- Literature review focusing on macrophage biology in atherosclerosis.
- Analysis of pro-inflammatory and anti-inflammatory factor effects on macrophage polarization and function.
- Synthesis of current understanding of macrophage-mediated lipid metabolism and plaque stability.
Main Results:
- Pro-inflammatory factors promote M1 macrophage polarization, lipid accumulation, and foam cell formation, driving AS.
- Anti-inflammatory factors induce M2 macrophage polarization, promoting tissue repair and plaque stabilization.
- Macrophages regulate lipid metabolism and influence T-cell responses, impacting AS progression.
Conclusions:
- Macrophages play a dual role in AS, with M1 promoting inflammation and M2 mediating resolution.
- Targeting macrophage polarization and function presents a promising strategy for managing AS.
- Further research into macrophage-centric mechanisms can yield novel diagnostic and therapeutic approaches for AS.
Abstract:
Atherosclerosis (AS) is an important pathological basis for the occurrence of Coronary Atherosclerotic Disease (CAD), stroke and other adverse cardiovascular events. AS is an inflammatory disease, and macrophages are the main inflammatory cells in AS lesions, playing a leading role in the formation of atherosclerotic plaques and the development and regression of AS. Various proinflammatory and anti-inflammatory factors act on macrophages to regulate AS. Pro-inflammatory factors recruit monocytes to accumulate in the inflammatory site and promote the transformation of monocytes to macrophages. A large number of aggregated macrophages secrete various inflammatory mediators to promote AS. Pro-inflammatory factors can induce the polarization of M1-type macrophages to start and maintain inflammation, promote the accumulation of lipids in macrophages, and accelerate the formation of foam cells. Anti-inflammatory factors can not only induce M2-type macrophages polarization, promote tissue remodeling and repair, and reduce the occurrence of AS, but also promote the metabolism of fatty acid oxidation and oxidative phosphorylation of macrophages, regulate lipid metabolism, stabilize plaques, and induce the transformation of helper T cells of type 1/2 (Th1/Th2) to Th2 cells, thus reducing inflammation. This review summarizes the effect and underlying regulatory mechanism of macrophages in the development of AS, which can provide new ideas for the diagnosis and treatment of AS targeting macrophages.
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