内质网应激诱导自噬的分子机制及意义

The Molecular Mechanism and Significance of Autophagy Induced by Endoplasmic Reticulum Stress

细胞对内质网应激(endoplasmic reticulum stress,ER stress)的早期反应是启动未折叠反应(unfolded protein response,UPR),ER stress及UPR与人类多种疾病的发病机制相关。近年来的研究表明ER stress可诱导细胞自噬(autophagy)。内质网应激诱导的自噬反应既可以帮助细胞减轻ER stress反应,又可以引导细胞发生非凋亡性死亡。本文将对ER stress诱导自噬的分子机制及可能的临床意义进行阐述。

One of the early cellular responses to endoplasmic reticulum stress （ER stress） is the activation of the unfolded protein response （UPR）. ER stress and the UPR are both implicated in numerous human diseases and pathologies. Emerging data now indicate th- at ER stress is also a potent inducer of autophagy. Autophagy induced during ER stress results either in enhancing cell survival or in committing the cell to non-apoptotic death, Here, we discuss the signaling pathways linking ER stress to autophagy and possibilities for their clinical exploitation.