摘要
内质网应激(endoplasmic reticulum stress,ERs)是内质网腔内错误折叠蛋白聚积的一种适应性反应,适度ERs通过激活未折叠蛋白反应起适应性的细胞保护作用,而过高和持久的ERs则通过诱导转录因子CHOP表达、激活caspase-12和c-Jun氨基末端激酶(JNK)等导致细胞凋亡。近年来,越来越多的研究提示内质网应激是神经退行性病变、2型糖尿病以及肥胖等疾病发生过程中的重要环节。对内质网应激的细胞效应分子机制进行综述。随着对ERs机制理解的深入,有可能会发现新的分子标志物或新的诊疗策略。
Endoplasmic reticulum （ER） stress is an adaptive response to the accumulation of misfolded proteins within the ER, the moderate ER stress contributes to adaptive cytoprotection through the activation of unfolded protein response, while excessive and prolonged ER stress triggers cell apoptosis through inducing expression of transcription factor CHOP, and activating caspase-12 and c-Jun N-terminal kinase（JNK）, etc. In recent years, increasing evidences have shown that endoplasmic reticulum stress plays an important role in neurodegenerative diseases, type 2 diabetes and obesity, etc. Herein, we summarize cellular and molecular mechanisms of ER stress. Increasing our understanding of the mechanisms of ER stress could lead to the development of new biomarkers and to the discovery of new therapeutic strategies.
出处
《生命科学》
CSCD
2012年第3期287-291,共5页
Chinese Bulletin of Life Sciences
基金
科技部"十二五"科技重大专项基金(2012ZX09401-004)
关键词
内质网应激
未折叠蛋白反应
细胞凋亡
endoplasmic reticulum stress, unfolded protein response, apoptosis
