内质网应激与血管内皮细胞凋亡
首发时间:2013-07-09
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
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Endoplasmic reticulum stress and vascular endothelial cell apoptosis
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 ERS.Effective intervention of ERS against apoptosis has played the role of vascular endothelial protection. Here,we reviewed the recent 3 years' research progress of the mechanism for ERS involved in vascular endothelial cell apoptosis.
Keywords: apoptosis Endoplasmic reticulum stress vascular endothelial cell cell protection mechanism
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