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

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.

Automated summary

Atherosclerosis is a chronic vascular inflammatory disease, and macrophages in the plaque play a crucial role in immune response. The phenotype of plaque macrophages changes dynamically in response to the microenvironment of the plaque. Oxygen-rich microenvironment in early plaques promotes M2/alternatively activated macrophages through oxidative phosphorylation, while the hypoxic microenvironment in advanced plaques promotes M1/classically activated macrophages through anaerobic glycolysis. Additionally, angiogenesis in the adventitia of aged plaques leads to an increased proportion of M2/M1 macrophages. This review provides insights into the dynamic changes of plaque macrophages and the regulation of plaque oxygen content and immune metabolism, which may offer new targets for the treatment of atherosclerosis.