JAK2-STAT3信号通路与心肌缺血再灌注损伤的研究进展

    Research progress of JAK2-STAT3 signaling pathway and myocardial ischemia reperfusion injury

    • 摘要: 心肌缺血再灌注损伤(myocardial ischemia reperfusion injury,MIRI)是由于血流灌注减少引起心肌细胞短期内出现缺血、缺氧,恢复灌注后损伤反而加重的一种病理状态。MIRI的病理过程主要涉及炎症反应、氧化应激损伤、细胞凋亡、内皮细胞损伤、钙超载等。JAK2-STAT3信号通路作为细胞功能的通讯节点,参与组织的缺血、缺氧、氧化应激以及细胞的生长、增殖、凋亡及炎症等多种病理过程。研究证实,多种细胞因子及药物通过调控JAK2-STAT3信号通路发挥抗炎、抗氧化应激、抗凋亡及促进血管内皮新生等作用。本文对JAK2-STAT3信号通路与心肌缺血再灌注损伤的病理机制的相关性进行综述,以期为心肌缺血再灌注损伤提供新的治疗靶点。

       

      Abstract: Myocardial ischemia reperfusion injury (MIRI) is a pathological state in which myocardial cells suffer from ischemia and hypoxia in a short time due to reduced blood perfusion and the injury is aggravated after reperfusion. The pathological process of MIRI mainly involves inflammatory reaction, oxidative stress injury, apoptosis, endothelial cell injury and calcium overload. JAK2-STAT3 signaling pathway, as the communication node of cell function, participates in many pathological processes such as ischemia, hypoxia, oxidative stress, cell growth, proliferation, apoptosis and inflammation. Many cytokines and drugs have been shown to play anti-inflammatory, anti-oxidative, anti-death and endothelial growth promoting roles through JAK2-STAT3 signaling pathway. This review focuses on the relationship between JAK2-STAT3 signaling pathway and the pathological mechanism of myocardial ischemia reperfusion injury, with a view to providing a new therapeutic target for myocardial ischemia reperfusion injury.

       

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