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| Research progress on molecular mechanism of macrophage polarization in atherosclerosis |
| PENG Chaojie WU Linke WU Hong |
The Second Clinical Medical College, Henan University of Chinese Medicine, Henan Province, Zhengzhou 450000, China
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Abstract Macrophages are one of the important immune cells in the development of atherosclerosis, and their phenotype and function play an important role in the occurrence and development of atherosclerosis. M1-type macrophages, by destroying their mitochondrial function, promote glycolysis and the release of reactive oxygen species, interfere with the balance of lipid metabolism of macrophages, maintain and expand the inflammatory response, and reduce the ability of macrophages to eliminate phagocytic necrotic cells. Accelerate the formation of necrotic cores and the occurrence of unstable plaque rupture. M2 type macrophages can maintain the normal respiratory function of mitochondria, promote oxidative phosphorylation metabolism, enhance intracellular lipid outflow, reduce inflammatory reaction, repair damaged tissues, clean necrotic cells, maintain plaque stability, and inhibit the progression of atherosclerosis. At present, the drugs used to prevent and treat atherosclerosis also show the potential to regulate the polarization of macrophages. Therefore, to further explore and summarize the molecular mechanism and effective target of regulating macrophage polarization in the pathological process of atherosclerosis is the potential direction of in-depth research on effective measures to prevent and treat atherosclerosis.
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