Relationship between Endoplasmic Reticulum Stress and Autophagy
XU Qian1, XU Yinfeng2,YANG Jiejie1,WANG Bin3, HOU Lin1,LI Ning1*
ERS (endoplasmic reticulum stress) is a universal stress-defense mechanism in eukaryotic cells. When ERS appears, UPR (unfolded protein response) is initiated, enhancing the unfolded proteins folding and misfolded proteins degradation, to restore normal physiological functions of ER. Some stimuli that trigger ERS can also induce autophagy. As a conservative degradation mechanism of eukaryotic cells, autophagy can increase the degradation of misfolded proteins and reduce the ERS, playing an important role on the maintenance of ER homeostasis besides UPR. Studies have demonstrated that ERS and ERS-induced autophagy are closely related to the occurrence and development of many diseases. However, how ERS triggers autophagy, how autophagy feedback regulates ERS, how UPR correlates autophagy and the roles of regulatory mechanisms between each other in the development of related diseases have not been discussed and defined in detail. The comprehensive view of the correlated mechanism between ERS and autophagy is significant for elucidating the pathogenesis of related diseases. Therefore, this article reviews the relationship and regulatory mechanism between ERS and autophagy in order to provide new ideas for the research of related fields.
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