巨噬细胞
趋化因子
再灌注损伤
巨噬细胞极化
免疫系统
免疫学
炎症
缺血
细胞生物学
巨噬细胞炎性蛋白
趋化性
单核细胞
医学
受体
生物
体外
内科学
生物化学
作者
Qigang Zhuang,Mingyue Li,Desheng Hu,Junyi Li
标识
DOI:10.1016/j.molimm.2024.02.007
摘要
Myocardial ischemia-reperfusion injury (MIRI) is a complex process that occurs when blood flow is restored after myocardium infarction (MI) with exacerbated tissue damage. Macrophages, essential cell type of the immune response, play an important role in MIRI. Macrophage subpopulations, namely M1 and M2, are distinguished by distinct phenotypes and functions. In MIRI, macrophages infiltrate in infarcted area, shaping the inflammatory response and influencing tissue healing. Resident cardiac macrophages interact with monocyte-derived macrophages in MIRI, and influence injury progression. Key factors including chemokines, cytokines, and toll-like receptors modulate macrophage behavior in MIRI. This review aims to address recent findings on the classification and the roles of macrophages in the myocardium, spanning from MI to subsequent MIRI, and highlights various signaling pathways implicated in macrophage polarization underlining the complexity of MIRI. This article will shed light on developing advanced therapeutic strategies for MIRI management.
科研通智能强力驱动
Strongly Powered by AbleSci AI