蛋白激酶激活与心肌缺血/再灌注损伤。
Protein kinase activation and myocardial ischemia/reperfusion injury.
作者信息
Armstrong Stephen C
机构信息
Department of Pathology, James H Quillen College of Medicine, East Tennessee State University, PO Box 70568, Johnson City, TN 37614, USA.
出版信息
Cardiovasc Res. 2004 Feb 15;61(3):427-36. doi: 10.1016/j.cardiores.2003.09.031.
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.
心肌缺血及缺血/再灌注会激活多种蛋白激酶途径。蛋白激酶的激活可能会调节心肌细胞损伤的发生，以及通过缺血预处理和药物预处理减轻这种损伤。心肌缺血/再灌注可能激活的主要蛋白激酶途径包括：丝裂原活化蛋白激酶（MAP激酶）、细胞外信号调节激酶1/2（ERK 1/2）、应激活化蛋白激酶1/2（JNK 1/2）、p38丝裂原活化蛋白激酶α/β（p38 MAPKα/β）；细胞存活激酶Akt；以及钠氢交换体（NHE）激酶p90核糖体S6激酶（p90RSK）。文献并不支持缺血/再灌注在酪氨酸激酶Src和Lck的激活，或蛋白激酶C（PKC）的易位和激活中起作用。本综述将详细阐述这些蛋白激酶在心肌细胞因坏死和凋亡而死亡的发生过程中所起的作用，以及预处理对这种损伤的减轻作用。
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