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Endoplasmic Reticulum Stress Regulates Cell Autophagy and Apoptosis
Feng Mei1, Fu Lingling1, Zhang Weihua2, XuJin1*
1Department of Preventive Medicine, Medical School of Ningbo University, Ningbo 315211, China; 2Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Abstract: Endoplasmic reticulum (ER) is an important membranous organelle for protein synthesis， folding and secretion in eukaryotic cells. Endogenous or exogenous stimuli， however， can lead to an imbalance between the ER protein folding capacity and protein load， giving rise to an accumulation of unfolded or misfolded proteins in the ER lumen， a condition dubbed as ‘ER stress’. In an attempt to meet the increased folding demand， cells utilize a conserved signaling pathway， the unfolded protein response (UPR)， which is initially charged to restore the homeostasis of endoplasmic reticulum. If this mechanism fails， persistent ER stress will eventually cause this cytoprotective UPR to switch into a autophagy pathway or even a cell death pathway. In this paper， we reviewed recent studies on mechanisms of ER stress-induced autophagy and apoptosis， which may provide relevant information for the researchers.
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