Figure 1.

ER stress is related to cell fate in liver diseases. The accumulation of unfolded and/or misfolded proteins could activate UPR. The activation of UPR overcomes disadvantageous effects and restores ER homeostasis via several prosurvival mechanisms, including inhibiting the synthesis of proteins, increasing protein folding or posttranslational modification abilities, and degradation of unfolded or misfolded proteins by the ERAD system. On the contrary, there are some factors or pathway related to ER stress-mediated cell death, including the translation of GADD34 and CHOP, RIDD, and IRE1-activated p38 and JNK signaling.