软骨细胞中内质网应激信号通路的研究进展  

Research progress on endoplasmic reticulum stress signaling pathways in chondrocytes

作　　者：闻娟[1] 李煌[1] 

机构地区：[1]南京大学医学院附属南京市口腔医院正畸科,南京210093

出　　处：《国际口腔医学杂志》2012年第6期756-759,765,共5页International Journal of Stomatology

基　　金：国家自然科学基金资助项目(81070807)

摘　　要：内外环境多种刺激均可导致内质网中未折叠蛋白的积聚,引起细胞内的应激反应,改变细胞的功能和存活状态,这个过程称为内质网应激(ERS)。软骨细胞是关节软骨内唯一的细胞成分,低糖性损伤、白细胞介素-1β和一氧化氮以及一些药物均能使其发生ERS。ERS可引发蛋白激酶R样内质网调节激酶(PERK)、肌醇需酶(IRE)1和活化转录因子(ATF)6三条主要的信号通路构成未折叠的蛋白反应(UPR)。UPR中多种信号分子对软骨细胞的生长、程序性死亡以及软骨的炎症都有重要的影响,本文就ERS信号通路机制、PERK信号通路、IRE1信号通路和ATF6信号通路等研究进展作一综述。The endoplasmic reticulum is susceptible to various stresses that provoke the accumulation of unfolded proteins in it, inducing stress response in cells, and altering the growth and function of cells. This is the endoplasmic reticulum stress（ERS）. ERS will happen in chondrocytes, the only ceils in cartilage, ＇after exposing to glucose deprivation, interleukin-1β, nitric oxide and some drugs. ERS triggers an evolutionarily conserved series of signal transduction events, which constitutes the unfolded protein response （UPR）. The three major transducers of the UPR are inositol-requiring （IRE） l, protein kinase R-like endoplasmic reticulum kinase（PERK）, and activating transcription factor （ATF） 6. They trigger major signal pathways of UPR, which affect the growth, apoptosis of chondroeytes and the inflammation of cartilage. Advances in the research into ERS, PERK, IRE I and ATF6 signal pathways are reviewed in this article.

关 键 词：内质网应激 未折叠蛋白反应 软骨细胞 

分 类 号：R363[医药卫生—病理学]