Macrophage metabolic reprogramming and atherosclerotic plaque microenvironment: Fostering each other?

被引:18
作者
Xiao, Qi [1 ]
Hou, Rongyao [2 ]
Xie, Linlin [1 ]
Niu, Mengying [1 ]
Pan, Xudong [1 ]
Zhu, Xiaoyan [3 ]
机构
[1] Qingdao Univ, Dept Neurol, Affiliated Hosp, Qingdao, Peoples R China
[2] Qingdao Univ, Dept Neurol, Affiliated Hiser Hosp, Qingdao, Peoples R China
[3] Qingdao Univ, Dept Crit Care Med, Affiliated Hosp, Qingdao, Peoples R China
基金
中国国家自然科学基金;
关键词
atherosclerosis; macrophage; metabolic reprogramming; plaque microenvironment; FOAM CELL-FORMATION; CCAAT/ENHANCER-BINDING-PROTEINS; HYPOXIA-INDUCIBLE FACTOR; NITRIC-OXIDE; LIPID-METABOLISM; CHOLESTEROL EFFLUX; TARGETED DELIVERY; PYRUVATE-KINASE; ACTIVATION; IMMUNOMETABOLISM;
D O I
10.1002/ctm2.1257
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Macrophages are the central immune cells in atherosclerosis (AS) and play a critical role in the initiation, progression and invasion of atherosclerotic plaques. Metabolic reprogramming is a crucial feature that determines macrophage function and is driven by a combination of intrinsic alterations in macrophages and extrinsic factors such as cytokines acting in the plaque microenvironment. Intrinsic macrophage mechanisms activate signal transduction pathways that change metabolic enzyme activity, and the expression of metabolic regulators. Extrinsic signalling mechanisms involve lipids and cytokines in the microenvironment, promoting and amplifying macrophage metabolic reprogramming. This review describes the intrinsic and extrinsic mechanisms driving macrophage metabolic reprogramming in the AS microenvironment and the interplay of these metabolic rewires in the microenvironment. Moreover, we discuss whether targeting these different pathways to treat macrophage microenvironmental changes can alter the fate of the vulnerable plaques.
引用
收藏
页数:18
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