The Aryl Hydrocarbon Receptor, Epigenetics and the Aging Process
The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, classically associated with the regulation of xenobiotic metabolism in response to environmental toxins. In recent years, transgenic rodent models have implicated AhR in aging and longevity. Moreover, several AhR ligands...
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| Published in | The Journal of nutrition, health & aging Vol. 27; no. 4; pp. 291 - 300 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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Paris
Elsevier Masson SAS
01.04.2023
Springer Paris Springer Nature B.V |
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| Abstract | The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, classically associated with the regulation of xenobiotic metabolism in response to environmental toxins. In recent years, transgenic rodent models have implicated AhR in aging and longevity. Moreover, several AhR ligands, such as resveratrol and quercetin, are compounds proven to extend the lifespan of model organisms. In this paper, we first review AhR biology with a focus on aging and highlight several AhR ligands with potential anti-aging properties. We outline how AhR-driven expression of xenobiotic metabolism genes into old age may be a key mechanism through which moderate induction of AhR elicits positive benefits on longevity and healthspan. Furthermore, via integration of publicly available datasets, we show that liver-specific AhR target genes are enriched among genes subject to epigenetic aging. Changes to epigenetic states can profoundly affect transcription factor binding and are a hallmark of the aging process. We suggest that the interplay between AhR and epigenetic aging should be the subject of future research and outline several key gaps in the current literature. Finally, we recommend that a broad range of non-toxic AhR ligands should be investigated for their potential to promote healthspan and longevity. |
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| AbstractList | The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, classically associated with the regulation of xenobiotic metabolism in response to environmental toxins. In recent years, transgenic rodent models have implicated AhR in aging and longevity. Moreover, several AhR ligands, such as resveratrol and quercetin, are compounds proven to extend the lifespan of model organisms. In this paper, we first review AhR biology with a focus on aging and highlight several AhR ligands with potential anti-aging properties. We outline how AhR-driven expression of xenobiotic metabolism genes into old age may be a key mechanism through which moderate induction of AhR elicits positive benefits on longevity and healthspan. Furthermore, via integration of publicly available datasets, we show that liver-specific AhR target genes are enriched among genes subject to epigenetic aging. Changes to epigenetic states can profoundly affect transcription factor binding and are a hallmark of the aging process. We suggest that the interplay between AhR and epigenetic aging should be the subject of future research and outline several key gaps in the current literature. Finally, we recommend that a broad range of non-toxic AhR ligands should be investigated for their potential to promote healthspan and longevity. The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, classically associated with the regulation of xenobiotic metabolism in response to environmental toxins. In recent years, transgenic rodent models have implicated AhR in aging and longevity. Moreover, several AhR ligands, such as resveratrol and quercetin, are compounds proven to extend the lifespan of model organisms. In this paper, we first review AhR biology with a focus on aging and highlight several AhR ligands with potential anti-aging properties. We outline how AhR-driven expression of xenobiotic metabolism genes into old age may be a key mechanism through which moderate induction of AhR elicits positive benefits on longevity and healthspan. Furthermore, via integration of publicly available datasets, we show that liver-specific AhR target genes are enriched among genes subject to epigenetic aging. Changes to epigenetic states can profoundly affect transcription factor binding and are a hallmark of the aging process. We suggest that the interplay between AhR and epigenetic aging should be the subject of future research and outline several key gaps in the current literature. Finally, we recommend that a broad range of non-toxic AhR ligands should be investigated for their potential to promote healthspan and longevity.The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, classically associated with the regulation of xenobiotic metabolism in response to environmental toxins. In recent years, transgenic rodent models have implicated AhR in aging and longevity. Moreover, several AhR ligands, such as resveratrol and quercetin, are compounds proven to extend the lifespan of model organisms. In this paper, we first review AhR biology with a focus on aging and highlight several AhR ligands with potential anti-aging properties. We outline how AhR-driven expression of xenobiotic metabolism genes into old age may be a key mechanism through which moderate induction of AhR elicits positive benefits on longevity and healthspan. Furthermore, via integration of publicly available datasets, we show that liver-specific AhR target genes are enriched among genes subject to epigenetic aging. Changes to epigenetic states can profoundly affect transcription factor binding and are a hallmark of the aging process. We suggest that the interplay between AhR and epigenetic aging should be the subject of future research and outline several key gaps in the current literature. Finally, we recommend that a broad range of non-toxic AhR ligands should be investigated for their potential to promote healthspan and longevity. |
| Author | McClay, J.L. Dozmorov, M.G. Abudahab, Sara Deshpande, L.S. Price, E.T. |
| AuthorAffiliation | 2. Department of Biostatistics, School of Medicine, Virginia Commonwealth University, Richmond, Virginia, USA 4. Department of Neurology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA 1. Department of Pharmacotherapy and Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, USA 5. Department of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA 3. Department of Pathology, Virginia Commonwealth University, Richmond, VA, 23284, USA |
| AuthorAffiliation_xml | – name: 4. Department of Neurology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA – name: 1. Department of Pharmacotherapy and Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, USA – name: 3. Department of Pathology, Virginia Commonwealth University, Richmond, VA, 23284, USA – name: 2. Department of Biostatistics, School of Medicine, Virginia Commonwealth University, Richmond, Virginia, USA – name: 5. Department of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA |
| Author_xml | – sequence: 1 givenname: Sara surname: Abudahab fullname: Abudahab, Sara email: abudahabs@vcu.edu organization: Department of Pharmacotherapy and Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, USA – sequence: 2 givenname: E.T. surname: Price fullname: Price, E.T. organization: Department of Pharmacotherapy and Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, USA – sequence: 3 givenname: M.G. surname: Dozmorov fullname: Dozmorov, M.G. organization: Department of Biostatistics, School of Medicine, Virginia Commonwealth University, Richmond, Virginia, USA – sequence: 4 givenname: L.S. surname: Deshpande fullname: Deshpande, L.S. organization: Department of Neurology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA – sequence: 5 givenname: J.L. surname: McClay fullname: McClay, J.L. organization: Department of Pharmacotherapy and Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, USA |
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| CitedBy_id | crossref_primary_10_1186_s12964_024_01847_9 crossref_primary_10_3389_fcimb_2023_1279172 crossref_primary_10_3390_ijms25052962 crossref_primary_10_32388_N1SCBR_3 crossref_primary_10_3390_cells13151259 |
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| Title | The Aryl Hydrocarbon Receptor, Epigenetics and the Aging Process |
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