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Molecular regulation after mucosal injury and regeneration in ulcerative colitis

Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease with a complex etiology. Intestinal mucosal injury is an important pathological change in individuals with UC. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5+) intestinal stem cells (ISCs) exhibit self-renewal a...

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Autores principales: Zheng, Lie, Duan, Sheng-Lei, Wen, Xin-Li, Dai, Yan-Cheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9606627/
https://www.ncbi.nlm.nih.gov/pubmed/36310594
http://dx.doi.org/10.3389/fmolb.2022.996057
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author Zheng, Lie
Duan, Sheng-Lei
Wen, Xin-Li
Dai, Yan-Cheng
author_facet Zheng, Lie
Duan, Sheng-Lei
Wen, Xin-Li
Dai, Yan-Cheng
author_sort Zheng, Lie
collection PubMed
description Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease with a complex etiology. Intestinal mucosal injury is an important pathological change in individuals with UC. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5+) intestinal stem cells (ISCs) exhibit self-renewal and high differentiation potential and play important roles in the repair of intestinal mucosal injury. Moreover, LGR5+ ISCs are intricately regulated by both the Wnt/β-catenin and Notch signaling pathways, which jointly maintain the function of LGR5+ ISCs. Combination therapy targeting multiple signaling pathways and transplantation of LGR5+ ISCs may lead to the development of new clinical therapies for UC.
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spelling pubmed-96066272022-10-28 Molecular regulation after mucosal injury and regeneration in ulcerative colitis Zheng, Lie Duan, Sheng-Lei Wen, Xin-Li Dai, Yan-Cheng Front Mol Biosci Molecular Biosciences Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease with a complex etiology. Intestinal mucosal injury is an important pathological change in individuals with UC. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5+) intestinal stem cells (ISCs) exhibit self-renewal and high differentiation potential and play important roles in the repair of intestinal mucosal injury. Moreover, LGR5+ ISCs are intricately regulated by both the Wnt/β-catenin and Notch signaling pathways, which jointly maintain the function of LGR5+ ISCs. Combination therapy targeting multiple signaling pathways and transplantation of LGR5+ ISCs may lead to the development of new clinical therapies for UC. Frontiers Media S.A. 2022-10-13 /pmc/articles/PMC9606627/ /pubmed/36310594 http://dx.doi.org/10.3389/fmolb.2022.996057 Text en Copyright © 2022 Zheng, Duan, Wen 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 Molecular Biosciences
Zheng, Lie
Duan, Sheng-Lei
Wen, Xin-Li
Dai, Yan-Cheng
Molecular regulation after mucosal injury and regeneration in ulcerative colitis
title Molecular regulation after mucosal injury and regeneration in ulcerative colitis
title_full Molecular regulation after mucosal injury and regeneration in ulcerative colitis
title_fullStr Molecular regulation after mucosal injury and regeneration in ulcerative colitis
title_full_unstemmed Molecular regulation after mucosal injury and regeneration in ulcerative colitis
title_short Molecular regulation after mucosal injury and regeneration in ulcerative colitis
title_sort molecular regulation after mucosal injury and regeneration in ulcerative colitis
topic Molecular Biosciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9606627/
https://www.ncbi.nlm.nih.gov/pubmed/36310594
http://dx.doi.org/10.3389/fmolb.2022.996057
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