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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 stress (ERs) is an adaptive response to the accumulation of misfolded proteins in the endoplasmic reticulum. Moderate ERs respond to adaptive cytoprotection through activation of unfolded proteins, while excessive and long lasting ERs induce apoptosis by inducing transcription factor CHOP expression, activating caspase-12 and c-Jun N-terminal kinase (JNK). In recent years, more and more studies suggest that endoplasmic reticulum stress is an important link in the development of diseases such as neurodegenerative diseases, type 2 diabetes and obesity. The cellular mechanism of endoplasmic reticulum stress is reviewed. As the understanding of the mechanisms of ERs deepens, new molecular markers or new treatment strategies may be found.