Induction of JAK2/STAT3 pathway contributes to protective effects of different therapeutics against myocardial ischemia/reperfusion.

Navid Omidkhoda, Sina Mahdiani, Gholamreza Karimi, Ramin Rezaee, Shadi Heidari

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2022;155():113751

PMID: 36162372

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Abstract

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.

Address: Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.; Department of Clinical Pharmacy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.; Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.; Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran; Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: [email protected].

DOI: 10.1016/j.biopha.2022.113751

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MeSH Terms: Humans, Myocardial Reperfusion Injury, Reactive Oxygen Species, TYK2 Kinase, Janus Kinase 2, STAT3 Transcription Factor, Myocardial Ischemia, Myocardial Infarction, Apoptosis, Reperfusion