“… 66 Therefore, PERK plays an indispensable role in decreasing ERS through reducing the production of nascent proteins. ATF4 is a key gene for ERS-induced autophagy and apoptosis by activating these proteins, 67 , 68 such as C/EBP homologous protein (CHOP), 69 parkin, 70 and CD36, 71 et al The phosphorylated eIF2α can selectively activate ATF4, resulting in modulating amino acid transport, antioxidant defenses, and the biosynthesis of lipids the transcription factor. 52 , 72 Notably, when the ERS persists continuously, autophagy is defined as the last guardian to restore the homeostasis of ER through engulfing the damaged ER 73 ( Figure 1 ).…”