内质网应激与血管内皮细胞凋亡.doc

文档介绍：
内质网应激与血管内皮细胞凋亡#
邱志凌1,张军平2,郭晓辰2**
(1. 天津中医药大学研究生院,天津 300193;
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2. 天津中医药大学第一附属医院,天津 300193)
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。虽然其早期通过激活未折叠蛋白反应(UPR)使细胞内蛋白质合成暂停,恢
复内质网稳态,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 CHOP、JNK 及 Caspases 等通路诱导细胞凋亡。近年来研究发现,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。
本文就近 3 年来对于 ERS 参与血管内皮细胞凋亡机制的研究进展作简要综述。
关键词:细胞凋亡;内质网应激;血管内皮细胞;细胞保护;机制
中图分类号:+8
Endoplasmic reticulum stress and vascular endothelial cell
apoptosis
QIU Zhiling1, ZHANG Junping2, GUO Xiaochen2
(1. Graduate School,Tianjin University of Chinese Medicine, TianJin 300193;
2. the First Affiliated Hospital, Tianjin University of Chinese Medicine, TianJin 300193)
Abstract: Endoplasmic reticulum stress (ERS) is a new discovery pathway following the death
receptor signaling pathway and the mitochondrial pathway of apoptosis. Although by activating
the unfolded protein response (UPR) it can suspend protein synthesis, restore the endoplasmic
reticulum homeostasis, play a role in cell protection. But as the inducing factors of ERS persist,
ERS will also be ongoing, triggering CHOP, JNK, Caspases or other pathways to induce apoptosis.
Recent studies found that the vascular endothelial cell apoptosis is closely related with the
intervention of ERS against apoptosis has played the role of vascular endothelial