摘要
内质网应激(ERS)凋亡途径是继死亡受体信号途径和线粒体途径后发现的一种新的细胞凋亡途径。虽然该途径早期通过激活未折叠蛋白反应使细胞内蛋白质合成暂停、内质网稳态恢复,起到细胞保护作用,但当机体诱导ERS的因素持续存在,ERS也将持续进行,并会触发C/EBP同源蛋白、c-JUN氨基末端激酶及caspase等通路诱导细胞凋亡。血管内皮细胞损伤及凋亡是各种疾病和病理生理过程的重要环节,大量研究表明,血管内皮细胞凋亡与ERS密切相关,通过干预ERS可以有效对抗其凋亡,起到保护血管内皮的作用。本文总结了ERS及其参与血管内皮细胞凋亡机制的研究进展。
Endoplasmic reticulum stress （ERS） is a new pathway of apoptosis following the discovery of death receptor signaling pathway and mitochondrial pathway. By activating the unfolded protein response （UPR）, ERS can suspend protein synthesis, restore the endoplasmic reticulum homeostasis, and thus play a protective role for cells; however, if the inducing factors of ERS persist, ERS will continue to trigger C/EBP homologous protein, JNK, caspase, or other pathways to induce apoptosis. In addition, the injury and apoptosis of vascular endothelial cells are key links in various diseases and pathophysiologic processes, and research has also shown that vascular endothelial cell apoptosis is closely related with the ERS. Effective intervention of ERS may restrain apoptosis and protect the vascular endothelium. This article reviews the recent research advances in ERS and its role in vascular endothelial cell apoptosis.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
2014年第1期102-107,共6页
Acta Academiae Medicinae Sinicae
基金
高等学校博士学科点专项科研基金(20121210110002)~~
关键词
内质网应激
血管内皮细胞
凋亡
细胞保护
机制
endoplasmic reticulum stress
vascular endothelial cell
apoptosis
cell protection
mechanism
