巨噬细胞极化
巨噬细胞
发病机制
表型
M2巨噬细胞
免疫学
医学
生物
体外
基因
遗传学
作者
Sai Yang,Hou‐Qin Yuan,Yameng Hao,Zhong Ren,Shun-Lin Qu,Lu‐Shan Liu,Dangheng Wei,Zhi-Han Tang,Jifeng Zhang,Zhisheng Jiang
标识
DOI:10.1016/j.cca.2019.10.034
摘要
Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization.
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