p38和JNK在肝脏缺血再灌注中的作用。
Role of p38 and JNK in liver ischemia and reperfusion.
作者信息
King LaShonda A, Toledo Alexander H, Rivera-Chavez Fernando A, Toledo-Pereyra Luis H
机构信息
Department of Research, Kalamazoo Center for Medical Studies, Michigan State University, 1000 Oakland Drive, Kalamazoo, MI 49008, USA.
出版信息
J Hepatobiliary Pancreat Surg. 2009;16(6):763-70. doi: 10.1007/s00534-009-0155-x. Epub 2009 Aug 13.
BACKGROUND/PURPOSE: The signal transduction of mitogen-activated protein kinases (MAPKs) has appeared to be an important mediator of ischemic-related events. Because of this, we analyzed the participation of p38 and JNK in liver ischemia and reperfusion, as two individual members of the MAPK family of proteins.
METHODS
All papers referred to in PubMed for the past 15 years were analyzed to determine how and when these MAPKs were considered to be an intricate part of the ischemic event. References were cross-studied to ascertain whether other papers could be found in the literature.
RESULTS
The role of p38 and JNK in liver ischemia was confirmed in the literature. The activation of these mediators was associated with the induction of apoptosis and necrosis. Inhibitors of p38 and JNK reduced the liver ischemia and reperfusion damage, probably through the mechanisms mentioned before.
CONCLUSIONS
The development of effective inhibitors of p38 and JNK protein mediators is important for minimizing the harmful effects associated with liver ischemia and reperfusion.
背景/目的：丝裂原活化蛋白激酶（MAPKs）的信号转导似乎是缺血相关事件的重要介质。因此，我们分析了p38和JNK作为MAPK蛋白家族的两个独立成员在肝脏缺血再灌注中的参与情况。
方法
分析过去15年PubMed中引用的所有论文，以确定这些MAPKs如何以及何时被视为缺血事件的复杂组成部分。对参考文献进行交叉研究，以确定文献中是否能找到其他论文。
结果
文献证实了p38和JNK在肝脏缺血中的作用。这些介质的激活与细胞凋亡和坏死的诱导有关。p38和JNK的抑制剂可能通过上述机制减轻肝脏缺血再灌注损伤。
结论
开发有效的p38和JNK蛋白介质抑制剂对于将与肝脏缺血再灌注相关的有害影响降至最低至关重要。
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