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Cardiovascular Research 2004 61(3):427-436; doi:10.1016/j.cardiores.2003.09.031
© 2004 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Protein kinase activation and myocardial ischemia/reperfusion injury

Stephen C Armstrong*

Department of Pathology, James H Quillen College of Medicine, East Tennessee State University, P.O. Box 70568, Johnson City, TN 37614, USA

* Tel.: +1-423-439-6210; fax: +1-423-439-8060. armstron{at}mail.etsu.edu

Myocardial ischemia and ischemia/reperfusion activate several protein kinase pathways. Protein kinase activation potentially regulates the onset of myocardial cell injury and the reduction of this injury by ischemic and pharmacologic preconditioning. The primary protein kinase pathways that are potentially activated by myocardial ischemia/reperfusion include: the MAP kinases, ERK 1/2, JNK 1/2, p38 MAPK{alpha}/β; the cell survival kinase, Akt; and the sodium–hydrogen exchanger (NHE) kinase, p90RSK. The literature does not support a role for ischemia/reperfusion in the activation of the tyrosine kinases, Src and Lck, or the translocation and activation of PKC. This review will detail the role of these protein kinases in the onset of myocardial cell death by necrosis and apoptosis and the reduction of this injury by preconditioning.

KEYWORDS Protein kinases; Cardiomyocytes; Ischemia; Necrosis; Apoptosis

Time for primary review 20 days


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