Endoplasmic Reticulum Stress of Gut Enterocyte and Intestinal Diseases

Abstract

The endoplasmic reticulum, a vast reticular membranous network from the nuclear envelope to the plasma membrane responsible for the synthesis, maturation, and trafficking of a wide range of proteins, is considerably sensitive to changes in its luminal homeostasis. The loss of ER luminal homeostasis leads to abnormalities referred to as endoplasmic reticulum (ER) stress. Thus, the cell activates an adaptive response known as the unfolded protein response (UPR), a mechanism to stabilize ER homeostasis under severe environmental conditions. ER stress has recently been postulated as a disease research breakthrough due to its significant role in multiple vital cellular functions. This has caused numerous reports that ER stress-induced cell dysfunction has been implicated as an essential contributor to the occurrence and development of many diseases, resulting in them targeting the relief of ER stress. This review aims to outline the multiple molecular mechanisms of ER stress that can elucidate ER as an expansive, membrane-enclosed organelle playing a crucial role in numerous cellular functions with evident changes of several cells encountering ER stress. Alongside, we mainly focused on the therapeutic potential of ER stress inhibition in gastrointestinal diseases such as inflammatory bowel disease (IBD) and colorectal cancer. To conclude, we reviewed advanced research and highlighted future treatment strategies of ER stress-associated conditions.

Peculiarities of Endoplasmic Reticulum Stress Regulator XBP1 Expression in the Gut-Associated Lymphoid Tissue of Wistar Rats under Chronic Stress

“…There is interesting data on the presence of a functional connection between ERS and chronic social stress, in particular, a number of works have shown the relationship of the "response to uncon verted proteins" system with the development of stress induced depression and cognitive disorders in rats [15][16][17], and changes in the expression level of key regulators PERK, IRE1a and ATF6a induced apoptosis development under chronic social stress [18,19]. This, in turn, suggests the involvement of ERS in the development and pro gression of inflammatory and autoimmune dis eases under conditions of chronic social stress (CSS).…”

Mogroside V reduced the excessive endoplasmic reticulum stress and mitigated the Ulcerative colitis induced by dextran sulfate sodium in mice

“…ERS plays a crucial role in the pathogenesis and development of colitis [ 14 , 29 ]. The enhanced and dysregulated ERS response in intestinal tissues of colitis patients is closely associated with various pathophysiological processes, including intestinal mucosal barrier damage, inflammatory cell infiltration, and apoptotic cell death [ 30 , 31 ].…”

Effects of Different Spectrum of LEDs on Retinal Degeneration Through Regulating Endoplasmic Reticulum Stress

“… 54 However, ER stress can be prolonged and induce ER stress-induced apoptosis if the UPR fails to recover ER function. 55 , 56 ATF4, a downstream molecule of the ER protein sensor PERK, is an essential mediator of ER stress-induced apoptosis 57 ; and CHOP is a crucial member of the enhancer-binding protein family induced by ER stress and can be elevated by the PERK-ATF4 pathway to mediate apoptosis. 58 Changes in the expression levels of both may indicate ER stress.…”