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Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium
Cell death mechanisms have been associated with the development of inflammatory bowel diseases in humans and mice. Recent studies suggested that a complex crosstalk between autophagy/apoptosis, microbe sensing, and enhanced endoplasmic reticulum stress in the epithelium could play a critical role in...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121991/ https://www.ncbi.nlm.nih.gov/pubmed/25126549 http://dx.doi.org/10.1155/2014/218493 |
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author | Nunes, Tiago Bernardazzi, Claudio de Souza, Heitor S. |
author_facet | Nunes, Tiago Bernardazzi, Claudio de Souza, Heitor S. |
author_sort | Nunes, Tiago |
collection | PubMed |
description | Cell death mechanisms have been associated with the development of inflammatory bowel diseases in humans and mice. Recent studies suggested that a complex crosstalk between autophagy/apoptosis, microbe sensing, and enhanced endoplasmic reticulum stress in the epithelium could play a critical role in these diseases. In addition, necroptosis, a relatively novel programmed necrosis-like pathway associated with TNF receptor activation, seems to be also present in the pathogenesis of Crohn's disease and in specific animal models for intestinal inflammation. This review attempts to cover new data related to cell death mechanisms and inflammatory bowel diseases. |
format | Online Article Text |
id | pubmed-4121991 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-41219912014-08-14 Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium Nunes, Tiago Bernardazzi, Claudio de Souza, Heitor S. Biomed Res Int Review Article Cell death mechanisms have been associated with the development of inflammatory bowel diseases in humans and mice. Recent studies suggested that a complex crosstalk between autophagy/apoptosis, microbe sensing, and enhanced endoplasmic reticulum stress in the epithelium could play a critical role in these diseases. In addition, necroptosis, a relatively novel programmed necrosis-like pathway associated with TNF receptor activation, seems to be also present in the pathogenesis of Crohn's disease and in specific animal models for intestinal inflammation. This review attempts to cover new data related to cell death mechanisms and inflammatory bowel diseases. Hindawi Publishing Corporation 2014 2014-07-14 /pmc/articles/PMC4121991/ /pubmed/25126549 http://dx.doi.org/10.1155/2014/218493 Text en Copyright © 2014 Tiago Nunes et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Nunes, Tiago Bernardazzi, Claudio de Souza, Heitor S. Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium |
title | Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium |
title_full | Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium |
title_fullStr | Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium |
title_full_unstemmed | Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium |
title_short | Cell Death and Inflammatory Bowel Diseases: Apoptosis, Necrosis, and Autophagy in the Intestinal Epithelium |
title_sort | cell death and inflammatory bowel diseases: apoptosis, necrosis, and autophagy in the intestinal epithelium |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121991/ https://www.ncbi.nlm.nih.gov/pubmed/25126549 http://dx.doi.org/10.1155/2014/218493 |
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