Insufficiency in coronary blood supply results in myocardial ischemia and consequently, various clinical syndromes and irreversible injuries. Myocardial damage occurs as a result of two processes during acute myocardial infarction (MI): ischemia and subsequent reperfusion. According to the available evidence, oxidative stress, excessive inflammation reaction, reactive oxygen species (ROS) generation, and apoptosis are crucial players in the pathogenesis of myocardial ischemia/reperfusion (IR) injury. There is emerging evidence that Janus tyrosine kinase 2 (JAK2) signal transducer and activator of the transcription 3 (STAT3) pathway offers cardioprotection against myocardial IR injury. This article reviews therapeutics that exert cardioprotective effects against myocardial IR injury through induction of JAK2/STAT3 pathway.

冠状动脉供血不足会导致心肌缺血，从而导致各种临床综合征和不可逆的损伤。心肌损伤是急性心肌梗死 (MI) 期间两个过程的结果：缺血和随后的再灌注。根据现有证据，氧化应激、过度炎症反应、活性氧 (ROS) 生成和细胞凋亡是心肌缺血/再灌注 (IR) 损伤发病机制中的关键因素。越来越多的证据表明，Janus 酪氨酸激酶 2 (JAK2) 信号转导和转录 3 (STAT3) 通路的激活剂对心肌 IR 损伤具有心脏保护作用。本文回顾了通过诱导 JAK2/STAT3 通路对心肌 IR 损伤发挥心脏保护作用的治疗方法。