氧诱导巨噬细胞的代谢重编程在动脉粥样硬化斑块动态变化中的作用。

The role of metabolic reprogramming of oxygen-induced macrophages in the dynamic changes of atherosclerotic plaques.

作者信息

Shen Lin, Chen Weiyue, Ding Jiayi, Shu Gaofeng, Chen Minjiang, Zhao Zhongwei, Xia Shuiwei, Ji Jiansong

机构信息

Key Laboratory of Imaging Diagnosis and Minimally Invasive Intervention Research, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Department of Interventional Radiology, Clinical College of the Affiliated Central Hospital of Lishui University, Lishui, China.

出版信息

FASEB J. 2023 Mar;37(3):e22791. doi: 10.1096/fj.202201486R.

DOI:10.1096/fj.202201486R

PMID:36723768

Abstract

Atherosclerosis (As) is a chronic vascular inflammatory disease. Macrophages are the most important immune cells in atherosclerotic plaques, and the phenotype of plaque macrophages shifts dynamically to adapt to changes in the plaque microenvironment. The aerobic microenvironment of early atherosclerotic plaques promotes the transformation of M2/alternatively activated macrophages mainly through oxidative phosphorylation; the anoxic microenvironment of advanced atherosclerotic plaques mainly promotes the formation of M1/classically activated macrophages through anaerobic glycolysis; and the adventitia angiogenesis of aged atherosclerotic plaques leads to an increase in the proportion of M2/M1 macrophages. Therefore, this review deeply elucidates the dynamic change mechanism of plaque macrophages and the regulation of plaque oxygen content and immune metabolism to find new targets for the treatment of As.

摘要

动脉粥样硬化（As）是一种慢性血管炎症性疾病。巨噬细胞是动脉粥样硬化斑块中最重要的免疫细胞，斑块巨噬细胞的表型会动态转变以适应斑块微环境的变化。早期动脉粥样硬化斑块的有氧微环境主要通过氧化磷酸化促进M2/替代性活化巨噬细胞的转变；晚期动脉粥样硬化斑块的缺氧微环境主要通过无氧糖酵解促进M1/经典活化巨噬细胞的形成；而老化动脉粥样硬化斑块的外膜血管生成导致M2/M1巨噬细胞比例增加。因此，本综述深入阐明了斑块巨噬细胞的动态变化机制以及斑块氧含量和免疫代谢的调节，以寻找As治疗的新靶点。