程序性坏死机制与缺血再灌注损伤

基础医学与临床 ›› 2014, Vol. 34 ›› Issue (3): 414-417.

程序性坏死机制与缺血再灌注损伤

叶周恒¹,刘文武¹,孙学军²

1. 第二军医大学
2. 第二军医大学海军医学系

收稿日期:2013-06-13 修回日期:2013-09-25 出版日期:2014-03-05 发布日期:2014-02-27
通讯作者: 孙学军 E-mail:power_1943@126.com

Molecular Mechanism of Necroptosis and its Effect in IR injury

Received:2013-06-13 Revised:2013-09-25 Online:2014-03-05 Published:2014-02-27
Contact: Xue-jun SUN E-mail:power_1943@126.com

摘要/Abstract

摘要： 程序性坏死是一种具有可调控的信号转导通路的细胞坏死方式。多种刺激可导致程序性坏死的发生，复合体I、复合体II和RIP1-RIP3坏死体是通路中的信号分子，而Necstatin-1是程序性坏死的特异性阻断剂。程序性坏死可能是缺血再灌注损伤中细胞死亡的重要方式。

关键词: 程序性坏死, 受体相互作用蛋白激酶1, 受体相互作用蛋白激酶3

Abstract: Necroptosis is a special cell necrosis that is capable of being regulated through particular molecular mechanism. Multiple stimuli could induce necroptosis , complex I, complex II and RIP1-RIP3 necrosome are critical participants in the necroptosis. Also, necrostatin-1 is a special and potent small-molecular inhibitor of necroptosis. Necroptosis could be an important alternative for cell death in ischemia-reperfusion injury.

Key words: Necroptosis, receptor interaction protein kinase 1, receptor interaction protein kinase 3

中图分类号:

叶周恒刘文武孙学军. 程序性坏死机制与缺血再灌注损伤[J]. 基础医学与临床, 2014, 34(3): 414-417.