Targeting mitochondrial function in macrophages: A novel treatment strategy for atherosclerotic cardiovascular disease?

传出细胞增多 炎症 氧化应激 线粒体 疾病 巨噬细胞 生物 巨噬细胞极化 免疫学 医学 细胞生物学 癌症研究 内科学 内分泌学 体外 生物化学
作者
Pierre-Hadrien Becker,Patrice Thérond,Pauline Gaignard
出处
期刊:Pharmacology & Therapeutics [Elsevier]
卷期号:247: 108441-108441 被引量:6
标识
DOI:10.1016/j.pharmthera.2023.108441
摘要

Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality due to chronic arterial injury caused by hyperlipidemia, hypertension, inflammation and oxidative stress. Recent studies have shown that the progression of this disease is associated with mitochondrial dysfunction and with the accumulation of mitochondrial alterations within macrophages of atherosclerotic plaques. These alterations contribute to processes of inflammation and oxidative stress. Among the many players involved, macrophages play a pivotal role in atherogenesis as they can exert both beneficial and deleterious effects due to their anti- and pro-inflammatory properties. Their atheroprotective functions, such as cholesterol efflux and efferocytosis, as well as the maintenance of their polarization towards an anti-inflammatory state, are particularly dependent on mitochondrial metabolism. Moreover, in vitro studies have demonstrated deleterious effects of oxidized LDL on macrophage mitochondrial function, resulting in a switch to a pro-inflammatory state and to a potential loss of atheroprotective capacity. Therefore, preservation of mitochondrial function is now considered a legitimate therapeutic strategy. This review focuses on the potential therapeutic strategies that could improve the mitochondrial function of macrophages, enabling them to maintain their atheroprotective capacity. These emerging therapies could play a valuable role in counteracting the progression of atherosclerotic lesions and possibly inducing their regression.
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