摘要
肝移植冷缺血再灌注(IR)可以引起肠黏膜充血性缺血和再灌注损伤,肠黏膜上皮细胞对于肠充血基础的缺血缺氧很敏感,这些细胞常会在术后发生凋亡或坏死。而程序性坏死是在凋亡受到抑制时,由死亡受体介导,调节细胞发育及组织平衡。受体交互蛋白1( RIPK1)大量聚集形成复合体Ⅱ,与RIPK3相互作用,是启动程序性坏死的关键。本文对程序性坏死在肝移植IR中的发生机制作一综述。
During liver transplantation, the anhepatic phase can induce ischemic reperfusion (IR) injury of the liver and therefore cause dysfunction of remote organs, especially gut. The IR can lead to intestine congestive ischemia and gastrointestinal congestion, which leads to intestinal injury. The epithelial cells of the intestinal mucosa are sensitive to the hypoxia-ischemia upon intestinal congestion, and they are often subjected to apoptosis and necrosis after surgery. Necroptosis is mediated by death receptor ligation when apoptotic pathway is inhibited. The complexⅡ, which is formed by increasing aggregation of receptor-interacting serine/threonine protein kinase 1 (RIPK1),and the interaction between RIPK1 and RIPK3 are the key elements for the activation of necroptosis signaling pathway. This article reviews the molecular mechanisms of necroptosis in IR of liver transplantation.
作者
王永旺
王清平
喻文立
杜洪印
WANG Yong-wang;WANG Qing-ping;YU Wen-li△;DU Hong-yin(Department of Anesthesiology, Tianjin First Center Hospital, Tianjin 300192, China)
出处
《天津医药》
CAS
北大核心
2019年第5期552-555,共4页
Tianjin Medical Journal
基金
天津市自然科学基金项目(17JCYBJC28000,18JCYBJC27500)
关键词
程序性坏死
肠损伤
受体交互蛋白
肝移植
necroptosis
intestinal injury
receptor-interacting protein
liver transplantation
