摘要
程序性细胞坏死是一种新发现的细胞死亡形式。这类死亡细胞形态类似坏死,而其死亡过程受胞内主动机制的调节,由此改变了坏死细胞不受内在机制调控的经典概念。当细胞膜上死亡受体与其配体结合,细胞内凋亡因子caspase-8被抑制时,激活受体相互作用蛋白(receptor interaction protein,RIPK1/RIPK3)激酶及关键底物——混合谱系激酶结构域样蛋白(mixed lineage kinase domain-like protein,MLKL)的信号通路,从而触发细胞发生程序性细胞坏死。后者参与多种疾病的病理过程,如肿瘤、免疫炎症、神经退行性疾病、脑缺血损伤等。本文就程序性细胞坏死的信号通路、重要调控分子及在神经损伤相关疾病致病机制进行综述,并对研究方法和分析工具药物进行了归纳总结。
Necroptosis is a newly discovered form of cell death.The morphology of these dead cells is similar to that of necrosis,and the process of their death is regulated by intracellular mechanisms,thus changing the classical concept that necrotic cells are not regulated by internal mechanisms.When the cell membrane death receptor binds to its ligand and the intracellular apoptotic factor caspase-8 is inhibited,the signaling pathway of the receptor interaction protein(RIPK1/RIPK3)and the key substrate--mixed lineage kinase domain-like protein(MLKL)will be activated,thereby triggering programmed cell necrosis.Necroptosis is involved in the pathological process of many diseases,such as tumors,inflammatory diseases,neurodegenerative diseases,cerebral ischemia injury,etc.In this paper,the signaling pathways,important regulatory molecules,and possible pathogenic mechanisms of programmed cell necrosis in the brain injury are reviewed.Besides,the research methods and analytical tools were also summarized.
作者
钱奕茗(综述)
孙凤艳(审校)
QIAN Yi-ming;SUN Feng-yan(Department of Neurobiology,School of Basic Medical Sciences,Fudan University,Shanghai 200032,China)
出处
《复旦学报（医学版）》
CAS
CSCD
北大核心
2021年第2期240-247,共8页
Fudan University Journal of Medical Sciences
基金
国家自然科学基金(81571197,91771268)。
作者简介
Corresponding author:孙凤艳,E-mail:fysun@shmu.edu.cn。
