摘要
内质网(endoplasmic reticulum,ER)应激是真核细胞的一种保护性应激反应,通过激活未折叠蛋白反应(unfoldedprotein response,UPR)来减少细胞内蛋白的异常聚集,从而起到细胞保护作用,而长期、严重的ER应激则会诱导细胞凋亡或死亡。能引起ER应激的因素很多,如基因突变或机体的状态改变包括氧化应激、缺血、营养不足、病毒感染和钙平衡失调等。近来研究发现,ER应激在机体的炎症反应中发挥重要作用,UPR与炎症反应通路之间通过多种机制相互偶联,参与多种炎症性疾病的发生发展。该文就近年来关于ER应激与炎症相关性的研究进展做一综述。
Endoplasmic reticulum （ER） stress is a phenomenon that occurs when excessive misfolded and unfolded proteins ac- cumulated in the ER lumen during biosynthesis. ER stress trig- gels a series of signaling and transcriptional events known as the unfolded protein response （UPR） to restore homeostasis in the ER, while severe and consistent ER stress can trigger cell apop- tosis. ER stress could be induced by many stimuli such as gene mutation, oxidative stress, ischemia, nutritional deficiency, vi- rus infection and calcium balance disorders. Recently, a grow-ing body of evidence suggested that the ER stress can initiate in- flammation, and the signalling pathways in the UPR and inflam- mation are interconnected through various mechanisms. ER stress is now thought to be fundamental in the pathogenesis of in- flammatory diseases. This review mainly summarizes recently re- ported discoveries concerning ER stress associated with inflam- mation.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2013年第6期756-760,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No 81173074)
教育部博士点科研基金资助项目(No 20093420110002
20113420110004)
安徽省自然科学基金资助项目(No 11040606Q14)
关键词
内质网应激
未折叠蛋白反应
信号通路
炎症
NF-ΚB
细胞凋亡
endoplasmic reticulum stress
unfolded protein re- sponse
signaling pathway
inflammation
NF-κB
apoptosis
