Protein kinase activation and myocardial ischemia/reperfusion injury

被引：284
作者：
Armstrong, SC [1 ]
机构：
[1] E Tennessee State Univ, James H Quillen Coll Med, Dept Pathol, Johnson City, TN 37614 USA
来源：
CARDIOVASCULAR RESEARCH | 2004年 / 61卷 / 03期
关键词：
protein kinases; cardiomyocytes; ischemia; necrosis; apoptosis;
D O I：
10.1016/j.cardiores.2003.09.031
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
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 MAPKalpha/beta; 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. (C) 2003 European Society of Cardiology. Published by Elsevier B.V All rights reserved.
引用
收藏
页码：427 / 436
页数：10
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