In eukaryotic cells, the aggregation of the endoplasmic reticulum (ER)-mediated unfolded or misfolded proteins leads to disruption of the ER homeostasis, which can trigger ER stress. To restore the ER homeostasis, the ER stress activates the intracellular signaling cascade from the ER to the nucleus, referred to as the unfolded protein response (UPR). Autophagy primitively portrayed as an evolutionarily conserved process is involved in cellular homeostasis by facilitating the lysosomal degradation pathway for the recycling and elimination of intracellular defective macromolecules and organelles. Autophagy is tightly regulated by the protective mechanism of UPR. The UPR and autophagy are interlinked, which indicates that the ER stress can not only induce autophagy but also suppress it. Here, we discuss the molecular mechanism of ER stress and autophagy and their induction and inhibition signaling network.
Part of the book: Endoplasmic Reticulum