巨噬细胞
重编程
缺血
心肌缺血
细胞生物学
医学
生物
化学
心脏病学
生物化学
细胞
体外
作者
Fan Ao-Di,Lin Han-Qing,Wang Xi-Zheng,Ke Yang,Guo Hong-Xin,Haixia Zhang,Guanwei Fan,Li-Lan
标识
DOI:10.1016/j.cellsig.2024.111370
摘要
Acute myocardial infarction (AMI) is the leading cause of death worldwide, and reperfusion therapy is a critical therapeutic approach to reduce myocardial ischemic injury and minimize infarct size. However, ischemia/reperfusion (I/R) itself also causes myocardial injury, and inflammation is an essential mechanism by which it leads to myocardial injury, with macrophages as crucial immune cells in this process. Macrophages are innate immune cells that maintain tissue homeostasis, host defence during pathogen infection, and repair during tissue injury. During the acute phase of I/R, M1-type macrophages generate a pro-inflammatory milieu, clear necrotic myocardial tissue, and further recruit mononuclear (CCR2
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