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The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe

In recent years, aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered to be involved in aging phenotypes across several species. This receptor is a highly conserved biosensor that is activated by numerous exogenous and endogenous molecules, including microbio...

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Autores principales: Ojo, Emmanuel S., Tischkau, Shelley A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8534784/
https://www.ncbi.nlm.nih.gov/pubmed/34685709
http://dx.doi.org/10.3390/cells10102729
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author Ojo, Emmanuel S.
Tischkau, Shelley A.
author_facet Ojo, Emmanuel S.
Tischkau, Shelley A.
author_sort Ojo, Emmanuel S.
collection PubMed
description In recent years, aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered to be involved in aging phenotypes across several species. This receptor is a highly conserved biosensor that is activated by numerous exogenous and endogenous molecules, including microbiota metabolites, to mediate several physiological and toxicological functions. Brain aging hallmarks, which include glial cell activation and inflammation, increased oxidative stress, mitochondrial dysfunction, and cellular senescence, increase the vulnerability of humans to various neurodegenerative diseases. Interestingly, many studies have implicated AhR signaling pathways in the aging process and longevity across several species. This review provides an overview of the impact of AhR pathways on various aging hallmarks in the brain and the implications for AhR signaling as a mechanism in regulating aging-related diseases of the brain. We also explore how the nature of AhR ligands determines the outcomes of several signaling pathways in brain aging processes.
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spelling pubmed-85347842021-10-23 The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe Ojo, Emmanuel S. Tischkau, Shelley A. Cells Review In recent years, aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered to be involved in aging phenotypes across several species. This receptor is a highly conserved biosensor that is activated by numerous exogenous and endogenous molecules, including microbiota metabolites, to mediate several physiological and toxicological functions. Brain aging hallmarks, which include glial cell activation and inflammation, increased oxidative stress, mitochondrial dysfunction, and cellular senescence, increase the vulnerability of humans to various neurodegenerative diseases. Interestingly, many studies have implicated AhR signaling pathways in the aging process and longevity across several species. This review provides an overview of the impact of AhR pathways on various aging hallmarks in the brain and the implications for AhR signaling as a mechanism in regulating aging-related diseases of the brain. We also explore how the nature of AhR ligands determines the outcomes of several signaling pathways in brain aging processes. MDPI 2021-10-13 /pmc/articles/PMC8534784/ /pubmed/34685709 http://dx.doi.org/10.3390/cells10102729 Text en © 2021 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
Ojo, Emmanuel S.
Tischkau, Shelley A.
The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe
title The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe
title_full The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe
title_fullStr The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe
title_full_unstemmed The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe
title_short The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe
title_sort role of ahr in the hallmarks of brain aging: friend and foe
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8534784/
https://www.ncbi.nlm.nih.gov/pubmed/34685709
http://dx.doi.org/10.3390/cells10102729
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