Macrophage Plasticity and Atherosclerosis Therapy.
Macrophage Plasticity and Atherosclerosis Therapy.
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巨噬细胞可塑性与动脉粥样硬化治疗
DOI：
10.3389/fmolb.2021.679797
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发表时间：
2021
影响因子：
5
通讯作者：
Guo SD
中科院分区：
文献类型：
--
作者：
Lin P;Ji HH;Li YJ;Guo SD
动脉粥样硬化是一种慢性疾病，始于单核细胞进入内皮下层，随后分化为巨噬细胞。巨噬细胞是动脉粥样硬化斑块中的主要免疫细胞，参与了动脉粥样硬化斑块的动态发展。动脉粥样硬化斑块巨噬细胞的生物学特性决定了病变的大小、组成和稳定性。动脉粥样硬化巨噬细胞的异质性和可塑性是近年来研究的热点。研究表明，动脉粥样硬化斑块微环境中的脂质、细胞因子、趋化因子等分子调节巨噬细胞表型，促使巨噬细胞向促动脉粥样硬化或抗动脉粥样硬化状态转变。值得注意的是，M1/M2的分类过于简化，仅代表巨噬细胞的两种极端状态。此外，在动脉粥样硬化中，M2巨噬细胞并不总是具有保护作用。了解巨噬细胞的表型多样性和功能可以揭示它们在动脉粥样硬化斑块中的作用。鉴于降脂治疗不能完全延缓动脉粥样硬化的进展，具有高度异质性和可塑性的巨噬细胞为动脉粥样硬化的消退带来了希望。本文就巨噬细胞的表型多样性及其在动态动脉粥样硬化斑块形成过程中的作用进行综述，并探讨以巨噬细胞微环境为靶点治疗动脉粥样硬化的可能性。
Atherosclerosis is a chronic disease starting with the entry of monocytes into the subendothelium and the subsequent differentiation into macrophages. Macrophages are the major immune cells in atherosclerotic plaques and are involved in the dynamic progression of atherosclerotic plaques. The biological properties of atherosclerotic plaque macrophages determine lesion size, composition, and stability. The heterogenicity and plasticity of atherosclerotic macrophages have been a hotspot in recent years. Studies demonstrated that lipids, cytokines, chemokines, and other molecules in the atherosclerotic plaque microenvironment regulate macrophage phenotype, contributing to the switch of macrophages toward a pro- or anti-atherosclerosis state. Of note, M1/M2 classification is oversimplified and only represent two extreme states of macrophages. Moreover, M2 macrophages in atherosclerosis are not always protective. Understanding the phenotypic diversity and functions of macrophages can disclose their roles in atherosclerotic plaques. Given that lipid-lowering therapy cannot completely retard the progression of atherosclerosis, macrophages with high heterogeneity and plasticity raise the hope for atherosclerosis regression. This review will focus on the macrophage phenotypic diversity, its role in the progression of the dynamic atherosclerotic plaque, and finally discuss the possibility of treating atherosclerosis by targeting macrophage microenvironment.