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Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces

Complex sphingolipids are essential structural components of intestinal membranes, providing protection and integrity to the intestinal mucosa and regulating intestinal absorption processes. The role of sphingolipid signaling has been established in numerous cellular events, including intestinal cel...

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Detalles Bibliográficos
Autores principales: Abdel Hadi, Loubna, Di Vito, Clara, Riboni, Laura
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4736332/
https://www.ncbi.nlm.nih.gov/pubmed/26880864
http://dx.doi.org/10.1155/2016/3827684
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author Abdel Hadi, Loubna
Di Vito, Clara
Riboni, Laura
author_facet Abdel Hadi, Loubna
Di Vito, Clara
Riboni, Laura
author_sort Abdel Hadi, Loubna
collection PubMed
description Complex sphingolipids are essential structural components of intestinal membranes, providing protection and integrity to the intestinal mucosa and regulating intestinal absorption processes. The role of sphingolipid signaling has been established in numerous cellular events, including intestinal cell survival, growth, differentiation, and apoptosis. A significant body of knowledge demonstrates that intestinal sphingolipids play a crucial role, as such and through their signaling pathways, in immunity and inflammatory disorders. In this review, we report on and discuss the current knowledge on the metabolism, signaling, and functional implications of sphingolipids in inflammatory bowel disease (IBD), focusing on the different aspects of sphingolipid actions on inflammatory responses and on the potential of sphingolipid-targeted molecules as anti-IBD therapeutic agents.
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spelling pubmed-47363322016-02-15 Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces Abdel Hadi, Loubna Di Vito, Clara Riboni, Laura Mediators Inflamm Review Article Complex sphingolipids are essential structural components of intestinal membranes, providing protection and integrity to the intestinal mucosa and regulating intestinal absorption processes. The role of sphingolipid signaling has been established in numerous cellular events, including intestinal cell survival, growth, differentiation, and apoptosis. A significant body of knowledge demonstrates that intestinal sphingolipids play a crucial role, as such and through their signaling pathways, in immunity and inflammatory disorders. In this review, we report on and discuss the current knowledge on the metabolism, signaling, and functional implications of sphingolipids in inflammatory bowel disease (IBD), focusing on the different aspects of sphingolipid actions on inflammatory responses and on the potential of sphingolipid-targeted molecules as anti-IBD therapeutic agents. Hindawi Publishing Corporation 2016 2016-01-05 /pmc/articles/PMC4736332/ /pubmed/26880864 http://dx.doi.org/10.1155/2016/3827684 Text en Copyright © 2016 Loubna Abdel Hadi et al. https://creativecommons.org/licenses/by/4.0/ 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
Abdel Hadi, Loubna
Di Vito, Clara
Riboni, Laura
Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces
title Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces
title_full Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces
title_fullStr Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces
title_full_unstemmed Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces
title_short Fostering Inflammatory Bowel Disease: Sphingolipid Strategies to Join Forces
title_sort fostering inflammatory bowel disease: sphingolipid strategies to join forces
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4736332/
https://www.ncbi.nlm.nih.gov/pubmed/26880864
http://dx.doi.org/10.1155/2016/3827684
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