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The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes
There is increasing evidence for the role of intestinal permeability as a contributing factor in the pathogenesis of diabetes; however, the molecular mechanisms are poorly understood. Advanced glycation endproducts, of both exogenous and endogenous origin, have been shown to play a role in diabetes...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836043/ https://www.ncbi.nlm.nih.gov/pubmed/35163688 http://dx.doi.org/10.3390/ijms23031766 |
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author | Snelson, Matthew Lucut, Elisa Coughlan, Melinda T. |
author_facet | Snelson, Matthew Lucut, Elisa Coughlan, Melinda T. |
author_sort | Snelson, Matthew |
collection | PubMed |
description | There is increasing evidence for the role of intestinal permeability as a contributing factor in the pathogenesis of diabetes; however, the molecular mechanisms are poorly understood. Advanced glycation endproducts, of both exogenous and endogenous origin, have been shown to play a role in diabetes pathophysiology, in part by their ligation to the receptor for advanced glycation endproducts (RAGE), leading to a proinflammatory signalling cascade. RAGE signalling has been demonstrated to play a role in the development of intestinal inflammation and permeability in Crohn’s disease and ulcerative colitis. In this review, we explore the role of AGE-RAGE signalling and intestinal permeability and explore whether activation of RAGE on the intestinal epithelium may be a downstream event contributing to the pathogenesis of diabetes complications. |
format | Online Article Text |
id | pubmed-8836043 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-88360432022-02-12 The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes Snelson, Matthew Lucut, Elisa Coughlan, Melinda T. Int J Mol Sci Review There is increasing evidence for the role of intestinal permeability as a contributing factor in the pathogenesis of diabetes; however, the molecular mechanisms are poorly understood. Advanced glycation endproducts, of both exogenous and endogenous origin, have been shown to play a role in diabetes pathophysiology, in part by their ligation to the receptor for advanced glycation endproducts (RAGE), leading to a proinflammatory signalling cascade. RAGE signalling has been demonstrated to play a role in the development of intestinal inflammation and permeability in Crohn’s disease and ulcerative colitis. In this review, we explore the role of AGE-RAGE signalling and intestinal permeability and explore whether activation of RAGE on the intestinal epithelium may be a downstream event contributing to the pathogenesis of diabetes complications. MDPI 2022-02-03 /pmc/articles/PMC8836043/ /pubmed/35163688 http://dx.doi.org/10.3390/ijms23031766 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Snelson, Matthew Lucut, Elisa Coughlan, Melinda T. The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes |
title | The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes |
title_full | The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes |
title_fullStr | The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes |
title_full_unstemmed | The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes |
title_short | The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes |
title_sort | role of age-rage signalling as a modulator of gut permeability in diabetes |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836043/ https://www.ncbi.nlm.nih.gov/pubmed/35163688 http://dx.doi.org/10.3390/ijms23031766 |
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