Department of Cardiovasology, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, China.
Operating Room, Zhucheng People's Hospital, Zhucheng, China.
Curr Pharm Biotechnol. 2021;22(15):2008-2018. doi: 10.2174/1389201022666210122142233.
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.
动脉粥样硬化（AS）是冠心病（CAD）、中风和其他不良心血管事件发生的重要病理基础。AS 是一种炎症性疾病，巨噬细胞是 AS 病变中的主要炎症细胞，在动脉粥样硬化斑块的形成和 AS 的发展和消退中起主导作用。各种促炎和抗炎因子作用于巨噬细胞，调节 AS。促炎因子募集单核细胞聚集在炎症部位，并促进单核细胞向巨噬细胞的转化。大量聚集的巨噬细胞分泌各种炎症介质，促进 AS 的发生。促炎因子可诱导 M1 型巨噬细胞极化，启动并维持炎症，促进巨噬细胞内脂质的积累，加速泡沫细胞的形成。抗炎因子不仅可以诱导 M2 型巨噬细胞极化，促进组织重塑和修复，减少 AS 的发生，还可以促进巨噬细胞脂肪酸氧化和氧化磷酸化代谢，调节脂质代谢，稳定斑块，并诱导辅助性 T 细胞 1/2 型（Th1/Th2）向 Th2 细胞的转化，从而减少炎症。本综述总结了巨噬细胞在 AS 发展中的作用及潜在调控机制，可为针对巨噬细胞的 AS 诊断和治疗提供新的思路。
