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心肌梗死后巨噬细胞的吞噬作用。

The phagocytic role of macrophage following myocardial infarction.

机构信息

Joint Laboratory for Translational Cancer Research of Chinese Medicine of the Ministry of Education of the People's Republic of China, Guangdong Key Laboratory for Translational Cancer Research of Chinese Medicine, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.

Guangdong-Hong Kong-Macau Joint Lab On Chinese Medicine and Immune Disease Research, Guangzhou Univ Chinese Med, Guangzhou, Guangdong, 510006, China.

出版信息

Heart Fail Rev. 2023 Jul;28(4):993-1007. doi: 10.1007/s10741-023-10314-5. Epub 2023 May 9.

DOI:10.1007/s10741-023-10314-5
PMID:37160618
Abstract

Myocardial infarction (MI) is one of the cardiovascular diseases with high morbidity and mortality. MI causes large amounts of apoptotic and necrotic cells that need to be efficiently and instantly engulfed by macrophage to avoid second necrosis. Phagocytic macrophages can dampen or resolve inflammation to protect infarcted heart. Phagocytosis of macrophages is modulated by various factors including proteins, receptors, lncRNA and cytokines. A better understanding of mechanisms in phagocytosis will be beneficial to regulate macrophage phagocytosis capability towards a desired direction in cardioprotection after MI. In this review, we describe the phagocytosis effect of macrophages and summarize the latest reported signals regulating phagocytosis after MI, which will provide a new thinking about phagocytosis-dependent cardiac protection after MI.

摘要

心肌梗死(MI)是一种发病率和死亡率都很高的心血管疾病。MI 会导致大量的细胞凋亡和坏死,这些细胞需要被巨噬细胞迅速有效地吞噬,以避免二次坏死。吞噬巨噬细胞可以减轻或消除炎症,从而保护梗死的心脏。巨噬细胞的吞噬作用受多种因素的调节,包括蛋白质、受体、lncRNA 和细胞因子。更好地了解吞噬作用的机制将有助于调节巨噬细胞的吞噬能力,使其朝着 MI 后心肌保护的理想方向发展。在这篇综述中,我们描述了巨噬细胞的吞噬作用,并总结了最近报道的调节 MI 后吞噬作用的信号,这将为 MI 后依赖吞噬作用的心脏保护提供新的思路。

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Ferroptotic cardiomyocyte-derived exosomes promote cardiac macrophage M1 polarization during myocardial infarction.铁死亡性心肌细胞来源的外泌体在心肌梗死后促进心肌巨噬细胞 M1 极化。
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