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Publication
Intestinal Epithelial Cell Endoplasmic Reticulum Stress and Inflammatory Bowel
Disease Pathogenesis: An Update Review.
Authors Ma X, Dai Z, Sun K, Zhang Y, Chen J, Yang Y, Tso P, Wu G, Wu Z
Submitted By Submitted Externally on 4/24/2018
Status Published
Journal Frontiers in immunology
Year 2017
Date Published
Volume : Pages 8 : 1271
PubMed Reference 29118753
Abstract The intestinal epithelial cells serve essential roles in maintaining intestinal
homeostasis, which relies on appropriate endoplasmic reticulum (ER) function for
proper protein folding, modification, and secretion. Exogenous or endogenous
risk factors with an ability to disturb the ER function can impair the
intestinal barrier function and activate inflammatory responses in the host. The
last decade has witnessed considerable progress in the understanding of the
functional role of ER stress and unfolded protein response (UPR) in the gut
homeostasis and its significant contribution to the pathogenesis of inflammatory
bowel disease (IBD). Herein, we review recent evidence supporting the viewpoint
that deregulation of ER stress and UPR signaling in the intestinal epithelium,
including the absorptive cells, Paneth cells, goblet cells, and enteroendocrine
cells, mediates the action of genetic or environmental factors driving colitis
in experimental animals and IBD patients. In addition, we highlight
pharmacologic application of chaperones or small molecules that enhance protein
folding and modification capacity or improve the function of the ER. These
molecules represent potential therapeutic strategies in the prevention or
treatment of IBD through restoring ER homeostasis in intestinal epithelial
cells.




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