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  

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

作　　者：詹雅清 赖汉津 沈建通[1] 温仕宏[1] 黄文起[1] Zhan Yaqing;Lai Hanjin;Shen Jiantong;Wen Shihong;Huang Wenqi(Department of Anesthesiology,the First Affiliated Hospital of Sun Yat-sen University,Guangzhou 510080,China)

机构地区：[1]中山大学附属第一医院麻醉科,广州510080

出　　处：《中华普通外科学文献（电子版）》2021年第3期224-228,共5页Chinese Archives of General Surgery(Electronic Edition)

基　　金：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)。

摘　　要：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.

关 键 词：程序性坏死 细胞死亡 缺血损伤 治疗策略 

分 类 号：R364[医药卫生—病理学]