Why the study?
Emerging evidence indicates the JAK2/STAT3 pathway offers cardioprotection against myocardial ischemia/reperfusion injury.
Do therapeutics that induce the JAK2/STAT3 pathway offer cardioprotection against myocardial ischemia/reperfusion injury?
Do therapeutics that induce the JAK2/STAT3 pathway offer cardioprotection against myocardial ischemia/reperfusion injury?
This review highlights the JAK2/STAT3 pathway as a crucial mechanistic target for therapeutics aimed at mitigating myocardial ischemia/reperfusion injury.
May identify JAK2/STAT3 inducers for cardioprotection; leaves open clinical translation pending prospective trials.
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.
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Mahdiani et al. (2022) studied this question.
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