摘要
坏死性凋亡是新近发现的一种具有坏死特征的细胞程序性死亡,主要由受体交互作用蛋白1、受体交互作用蛋白3及混合连接激酶结构域样蛋白活化介导。坏死性凋亡参与多种病理状态下的细胞死亡及炎症反应的激活。目前研究证实,坏死性凋亡涉及多种原因导致的急性肾损伤的发病机制。干预坏死性凋亡信号通路对肾脏具有抑制肾脏细胞死亡、限制炎症反应进展、改善肾功能等多种保护作用。深入研究坏死性凋亡的分子调控机制及其与急性肾损伤的关系,有助于为急性肾损伤的病理机制研究和临床防治提供新思路和方向。
Recent studies have discovered a genetically programmed pathway of necrosis,termed as necroptosis,which is mainly regulated by receptor interaction protein 1,receptor interaction protein 3 and mixed lineage kinase domain-like protein.Necroptosis plays a crucial pathogenic role in cell death and might lead to inflammation.Acute kidney injury is a common clinical syndrome in which necroptosis has been proved to be largely involved.Blocking necroptosis signaling pathways has protective effects on renal tubular cells and reduces inflammation,as well as improving renal function.Further study of the molecular regulation mechanism of necroptosis and its relationship with acute kidney injury may provide new approaches for the pathological research and clinical prevention and treatment of acute kidney injury.
作者
储岳宁
刘军
CHU Yuening;LIU Jun(Department of Nephrology,Shanghai General Hospital,School of Medicine,Shanghai Jiao Tong University,Shanghai 200080,China)
出处
《医学综述》
2018年第4期651-655,共5页
Medical Recapitulate
基金
上海市科学技术委员会科研计划项目(15ZR1433500)