Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
AMED-PRIME, Japan Agency for Medical Research and Development, Tokyo 100-0004, Japan.
J Biochem. 2020 Jul 1;168(1):1-6. doi: 10.1093/jb/mvaa051.
Myocardial infarction is one of the major causes of death worldwide. Many heart cells die during myocardial infarction through various processes such as necrosis, apoptosis, necroptosis, autophagy-related cell death, pyroptosis and ferroptosis. These dead cells in infarcted hearts expose the so-called 'eat-me' signals, such as phosphatidylserine, on their surfaces, enhancing their removal by professional and non-professional phagocytes. Clearance of dead cells by phagocytes in the diseased hearts plays a crucial role in the pathology of myocardial infarction by inhibiting the inflammatory responses caused by the leakage of contents from dead cells. This review focuses on the rapidly growing understanding of the molecular mechanisms of dead cell phagocytosis, termed efferocytosis, during myocardial infarction, which contributes to the pathophysiology of myocardial infarction.
心肌梗死是全球范围内主要的死亡原因之一。在心肌梗死过程中，许多心肌细胞通过坏死、凋亡、坏死性凋亡、自噬相关细胞死亡、细胞焦亡和铁死亡等多种途径死亡。梗死心脏中的这些死亡细胞在表面暴露所谓的“吃我”信号，如磷脂酰丝氨酸，从而增强其被专业和非专业吞噬细胞清除。吞噬细胞清除病变心脏中的死亡细胞通过抑制由死亡细胞内容物漏出引起的炎症反应，在心梗的病理生理学中起着至关重要的作用。本综述重点介绍了在心肌梗死后吞噬死亡细胞的分子机制，即噬亡作用的快速发展，该机制有助于心肌梗死的病理生理学。
