Cargando…

Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis

Ulcerative colitis (UC) is a chronic nonspecific inflammation that mainly affects the mucosa and submucosa of the rectum and colon. Numerous studies have shown that endoplasmic reticulum stress (ERS)-induced autophagy plays a vital role in the pathogenesis of UC. ERS is the imbalance of internal bal...

Descripción completa

Detalles Bibliográficos
Autores principales: Qiao, Dan, Zhang, Ziwei, Zhang, Yali, Chen, Qian, Chen, Yujun, Tang, Yingjue, Sun, Xiong, Tang, Zhipeng, Dai, Yancheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8473789/
https://www.ncbi.nlm.nih.gov/pubmed/34588980
http://dx.doi.org/10.3389/fphar.2021.697360
_version_ 1784575070237097984
author Qiao, Dan
Zhang, Ziwei
Zhang, Yali
Chen, Qian
Chen, Yujun
Tang, Yingjue
Sun, Xiong
Tang, Zhipeng
Dai, Yancheng
author_facet Qiao, Dan
Zhang, Ziwei
Zhang, Yali
Chen, Qian
Chen, Yujun
Tang, Yingjue
Sun, Xiong
Tang, Zhipeng
Dai, Yancheng
author_sort Qiao, Dan
collection PubMed
description Ulcerative colitis (UC) is a chronic nonspecific inflammation that mainly affects the mucosa and submucosa of the rectum and colon. Numerous studies have shown that endoplasmic reticulum stress (ERS)-induced autophagy plays a vital role in the pathogenesis of UC. ERS is the imbalance of internal balance caused by misfolded or unfolded proteins accumulated in the endoplasmic reticulum (ER).Excessive ERS triggers the unfolded protein response (UPR), an increase in inositol-requiring enzyme 1, and a Ca(2+) overload, which activates the autophagy pathway. Autophagy is an evolutionarily conserved method of cellular self-degradation. Dysregulated autophagy causes inflammation, disruption of the intestinal barrier, and imbalance of intestinal homeostasis, therefore increasing the risk of colonic diseases. This review summarizes the pathogenesis of ERS, UPR, and ERS-related autophagy in UC, providing potential new targets and more effective treatment options for UC.
format Online
Article
Text
id pubmed-8473789
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-84737892021-09-28 Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis Qiao, Dan Zhang, Ziwei Zhang, Yali Chen, Qian Chen, Yujun Tang, Yingjue Sun, Xiong Tang, Zhipeng Dai, Yancheng Front Pharmacol Pharmacology Ulcerative colitis (UC) is a chronic nonspecific inflammation that mainly affects the mucosa and submucosa of the rectum and colon. Numerous studies have shown that endoplasmic reticulum stress (ERS)-induced autophagy plays a vital role in the pathogenesis of UC. ERS is the imbalance of internal balance caused by misfolded or unfolded proteins accumulated in the endoplasmic reticulum (ER).Excessive ERS triggers the unfolded protein response (UPR), an increase in inositol-requiring enzyme 1, and a Ca(2+) overload, which activates the autophagy pathway. Autophagy is an evolutionarily conserved method of cellular self-degradation. Dysregulated autophagy causes inflammation, disruption of the intestinal barrier, and imbalance of intestinal homeostasis, therefore increasing the risk of colonic diseases. This review summarizes the pathogenesis of ERS, UPR, and ERS-related autophagy in UC, providing potential new targets and more effective treatment options for UC. Frontiers Media S.A. 2021-09-13 /pmc/articles/PMC8473789/ /pubmed/34588980 http://dx.doi.org/10.3389/fphar.2021.697360 Text en Copyright © 2021 Qiao, Zhang, Zhang, Chen, Chen, Tang, Sun, Tang and Dai. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Qiao, Dan
Zhang, Ziwei
Zhang, Yali
Chen, Qian
Chen, Yujun
Tang, Yingjue
Sun, Xiong
Tang, Zhipeng
Dai, Yancheng
Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis
title Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis
title_full Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis
title_fullStr Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis
title_full_unstemmed Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis
title_short Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis
title_sort regulation of endoplasmic reticulum stress-autophagy: a potential therapeutic target for ulcerative colitis
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8473789/
https://www.ncbi.nlm.nih.gov/pubmed/34588980
http://dx.doi.org/10.3389/fphar.2021.697360
work_keys_str_mv AT qiaodan regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT zhangziwei regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT zhangyali regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT chenqian regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT chenyujun regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT tangyingjue regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT sunxiong regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT tangzhipeng regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis
AT daiyancheng regulationofendoplasmicreticulumstressautophagyapotentialtherapeutictargetforulcerativecolitis