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The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration

While sensing the cell environment, the aryl hydrocarbon receptor (AHR) interacts with different pathways involved in cellular homeostasis. This review summarizes evidence suggesting that cellular regeneration in the context of aging and diseases can be modulated by AHR signaling on stem cells. New...

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Autor principal: Casado, Fanny L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4987465/
https://www.ncbi.nlm.nih.gov/pubmed/27563312
http://dx.doi.org/10.1155/2016/4389802
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author Casado, Fanny L.
author_facet Casado, Fanny L.
author_sort Casado, Fanny L.
collection PubMed
description While sensing the cell environment, the aryl hydrocarbon receptor (AHR) interacts with different pathways involved in cellular homeostasis. This review summarizes evidence suggesting that cellular regeneration in the context of aging and diseases can be modulated by AHR signaling on stem cells. New insights connect orphaned observations into AHR interactions with critical signaling pathways such as WNT to propose a role of this ligand-activated transcription factor in the modulation of cellular regeneration by altering pathways that nurture cellular expansion such as changes in the metabolic efficiency rather than by directly altering cell cycling, proliferation, or cell death. Targeting the AHR to promote regeneration might prove to be a useful strategy to avoid unbalanced disruptions of homeostasis that may promote disease and also provide biological rationale for potential regenerative medicine approaches.
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spelling pubmed-49874652016-08-25 The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration Casado, Fanny L. Stem Cells Int Review Article While sensing the cell environment, the aryl hydrocarbon receptor (AHR) interacts with different pathways involved in cellular homeostasis. This review summarizes evidence suggesting that cellular regeneration in the context of aging and diseases can be modulated by AHR signaling on stem cells. New insights connect orphaned observations into AHR interactions with critical signaling pathways such as WNT to propose a role of this ligand-activated transcription factor in the modulation of cellular regeneration by altering pathways that nurture cellular expansion such as changes in the metabolic efficiency rather than by directly altering cell cycling, proliferation, or cell death. Targeting the AHR to promote regeneration might prove to be a useful strategy to avoid unbalanced disruptions of homeostasis that may promote disease and also provide biological rationale for potential regenerative medicine approaches. Hindawi Publishing Corporation 2016 2016-08-03 /pmc/articles/PMC4987465/ /pubmed/27563312 http://dx.doi.org/10.1155/2016/4389802 Text en Copyright © 2016 Fanny L. Casado. 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
Casado, Fanny L.
The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration
title The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration
title_full The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration
title_fullStr The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration
title_full_unstemmed The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration
title_short The Aryl Hydrocarbon Receptor Relays Metabolic Signals to Promote Cellular Regeneration
title_sort aryl hydrocarbon receptor relays metabolic signals to promote cellular regeneration
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4987465/
https://www.ncbi.nlm.nih.gov/pubmed/27563312
http://dx.doi.org/10.1155/2016/4389802
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