在成年人体内，每天会有数十亿个细胞死亡和更新。在这个过程中，会产生许多凋亡细胞，并随后被吞噬细胞清除——这个过程被称为巨噬细胞摄取，它在组织稳态中起着至关重要的作用。巨噬细胞摄取是控制炎症过程的重要机制。高效的巨噬细胞摄取抑制了凋亡细胞/残骸的积累，并在坏死（继发坏死）开始之前维持了稳态，从而促进了炎症或损伤的发生。在巨噬细胞摄取过程中，线粒体分裂和氧化应激过程通过产生活性氧种和控制氧化应激而相互关联。自噬在抑制炎症和凋亡以及促进激活炎症细胞（特别是中性粒细胞和巨噬细胞）的摄取过程中起着重要作用。中性粒细胞的自噬是由吞噬病原体或激活模式识别受体引起的。自噬对于中性粒细胞的主要功能至关重要，包括颗粒释放、活性氧种产生、氧化应激以及中性粒细胞外环境因子的释放。巨噬细胞的摄取功能丧失是慢性炎症性疾病（包括动脉粥样硬化、心脏代谢病理、神经退行性疾病和癌症）发展和进展的关键机制。凋亡性巨噬细胞的摄取能力不良是动脉粥样硬化的严重性和斑块易破裂的决定因素。最近的结果表明，抑制巨噬细胞对心肌的摄取会减少修复性巨噬细胞对组织的浸润，从而减少氧化应激。激活的巨噬细胞在炎症的发展和解决中起着中心作用。通过巨噬细胞摄取来解决炎症是一种内源性过程，可以保护宿主组织免受长时间或过度炎症的侵害。因此，预测那些改善巨噬细胞摄取控制的治疗策略将减轻炎症并改善炎症的解决。因此，针对巨噬细胞摄取的治疗方法将成为治疗心血管和代谢疾病等慢性炎症状态的新途径。版权所有 © 2023 年。Elsevier Masson SAS出版。

In an adult human, billions of cells die and turn over daily. During this process, many apoptotic cells are produced and subsequently cleared by phagocytes - a process termed efferocytosis, which plays a critical role in tissue homeostasis. Efferocytosis is an important mechanism in the control of inflammatory processes. Efficient efferocytosis inhibits accumulation of apoptotic cells/debris and maintains homeostasis before the onset of necrosis (secondary necrosis), which promotes inflammation or injury. During efferocytosis, mitochondrial fission and the oxidative stress process are linked through reactive oxygen species production and oxidative stress control. Autophagy plays an important role in inhibiting inflammation and apoptosis, and in promoting efferocytosis by activated inflammatory cells, particularly neutrophils and macrophages. Autophagy in neutrophils is activated by phagocytosis of pathogens or activation of pattern recognition receptors. Autophagy is essential for major neutrophil functions, including degranulation, reactive oxygen species production, oxidative stress and release of neutrophil extracellular cytokines. Failed efferocytosis is a key mechanism driving the development and progression of chronic inflammatory diseases, including atherosclerosis, cardiometabolic pathology, neurodegenerative disease and cancer. Impairment of efferocytosis in apoptotic macrophages is a determinant of atherosclerosis severity and the vulnerability of plaques to rupture. Recent results suggest that inhibition of efferocytosis in the protection of the myocardium results in reduced infiltration of reparatory macrophages into the tissue, in association with oxidative stress reduction. Activated macrophages play a central role in the development and resolution of inflammation. The resolution of inflammation through efferocytosis is an endogenous process that protects host tissues from prolonged or excessive inflammation. Accordingly, therapeutic strategies that ameliorate efferocytosis control would be predicted to dampen inflammation and improve resolution. Thus, therapies targeting efferocytosis will provide a new means of treating and preventing cardiovascular and metabolic diseases involving the chronic inflammatory state.Copyright © 2023. Published by Elsevier Masson SAS.