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中华普通外科学文献(电子版) ›› 2021, Vol. 15 ›› Issue (03) : 224 -228. doi: 10.3877/cma.j.issn.1674-0793.2021.03.015

所属专题: 文献

综述

程序性坏死的发生机制及其在缺血损伤性疾病中的研究进展
詹雅清1, 赖汉津1, 沈建通1, 温仕宏1,(), 黄文起1   
  1. 1. 510080 广州,中山大学附属第一医院麻醉科
  • 收稿日期:2020-08-11 出版日期:2021-06-01
  • 通信作者: 温仕宏
  • 基金资助:
    国家自然科学基金面上项目(81772116); 广东省基础与应用基础研究基金项目(2019A1515010143)

Advances in the molecular mechanisms of necroptosis and its progression in organ ischemic injuries

Yaqing Zhan1, Hanjin Lai1, Jiantong Shen1, Shihong Wen1,(), Wenqi Huang1   

  1. 1. Department of Anesthesiology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
  • Received:2020-08-11 Published:2021-06-01
  • Corresponding author: Shihong Wen
引用本文:

詹雅清, 赖汉津, 沈建通, 温仕宏, 黄文起. 程序性坏死的发生机制及其在缺血损伤性疾病中的研究进展[J]. 中华普通外科学文献(电子版), 2021, 15(03): 224-228.

Yaqing Zhan, Hanjin Lai, Jiantong Shen, Shihong Wen, Wenqi Huang. Advances in the molecular mechanisms of necroptosis and its progression in organ ischemic injuries[J]. Chinese Archives of General Surgery(Electronic Edition), 2021, 15(03): 224-228.

程序性坏死(Necroptosis)是一种细胞非凋亡性的程序性死亡,主要由受体相互作用蛋白激酶1和3介导,为近年来细胞死亡研究领域的热点。程序性坏死可由细胞外炎症和促进细胞死亡的相关信号诱发,进一步介导细胞内坏死复合体的形成及相关蛋白激酶激活。明确程序性坏死的发生机制及其在围手术期缺血损伤性疾病中的作用,将有助于提高对细胞死亡及器官缺血损伤机制的认识,同时选择合适的临床治疗策略。

Necroptosis has distinct cellular features that are different from apoptosis and is mediated by the kinase activity of RIPK1 and RIPK3. Necroptosis can be triggered by extracellular stimuli known to activate inflammation and cell death and its intracellular signaling pathway involves necrosome formation and kinases activation. Exploring the underlying mechanisms of Necroptosis and its roles in organ ischemic injuries will help to improve the understanding of the pathophysiology of cell death and tissue injury. Meanwhile, Necroptosis inhibition has potential to be an effective and efficient treatment strategy in the future.

图1 缺血再灌注后细胞发生程序性坏死(Necroptosis)的机制 缺血损伤后,RIP1-RIP3-MLKL通路激活,活化的RIP3激活PGAM5,进而再上调RIP1和MLKL,因此RIP1-RIP3-MLKL-PGAM5之间存在正反馈回路;PGAM5激活后通过进一步激活DRP1促进线粒体分裂;RIP3也可通过ROS途径或通过激活CaMKⅡ促进细胞发生Necroptosis
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