Abstract
Despite many scientific studies on depression, there is no clear conception explaining the causes and mechanisms of depression development. Research conducted in recent years has shown that there is a strong relationship between depression and the endoplasmic reticulum (ER) stress. In order to restore ER homeostasis, the adaptive unfolded protein response (UPR) mechanism is activated. Research suggests that ER stress response pathways are continuously activated in patients with major depressive disorders (MDD). Therefore, it seems that the recommended drugs should reduce ER stress. A search is currently underway for drugs that will be both effective in reducing ER stress and relieving symptoms of depression.
Highlights
Depression (Latin depressio-depression, oppression) is a psychiatric disorder characterized by a pathologically low mood and a negative attitude towards oneself, one’s status in the real world, and one’s future [1]
IRE1 and PERK are involved in the activation of the pro-apoptotic JNK (c-JunNH2terminal kinase), and activating transcription factor 4 (ATF4) is responsible for the activation of the pro-apoptotic transcription factor CHOP [30,31]
A detailed understanding of the changes taking place in the endoplasmic reticulum (ER) in depression will allow us to understand the mechanism of its formation and lead to the development of an appropriate therapeutic procedure to slow down or stop this disease
Summary
Depression (Latin depressio-depression, oppression) is a psychiatric disorder characterized by a pathologically low mood (hypothimia) and a negative attitude towards oneself, one’s status in the real world, and one’s future [1]. Under conditions of the reticulum stress, BiP as a chaperone binds to misfolded proteins, releasing the transmembrane proteins IRE1, PERK, and ATF6. Life 2021, 11, 1376 phorylated form of eIF2a has a lower recognition of the AUG translation initiation codon, which causes the inhibition of protein synthesis depending on the presence of the cap, i.e., 7-methylguanosine [22] Such translation control helps to reduce the amount of misfolded proteins in the cell undergoing stress from the endoplasmic reticulum and allows it to survive. IRE1 and PERK are involved in the activation of the pro-apoptotic JNK (c-JunNH2terminal kinase), and ATF4 is responsible for the activation of the pro-apoptotic transcription factor CHOP (growth arrest and DNA-damage-inducible protein 153, GADD153 gene) [30,31]. If the stress of the endoplasmic reticulum is irreversible, the PERK-ATF4-CHOP pathway will allow DR5 mRNA to grow and accumulate in the ER
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