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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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Published in: | Cells (Basel, Switzerland) Switzerland), 2021-10, Vol.10 (10), p.2729 |
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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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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.</description><identifier>ISSN: 2073-4409</identifier><identifier>EISSN: 2073-4409</identifier><identifier>DOI: 10.3390/cells10102729</identifier><identifier>PMID: 34685709</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Aging ; Aging - metabolism ; AhR endogenous/exogenous ligands ; Alzheimer's disease ; Animals ; aryl hydrocarbon receptor ; Biosensors ; Blood-brain barrier ; Brain - metabolism ; brain aging hallmarks ; Brain diseases ; Brain Diseases - metabolism ; Brain Diseases - pathology ; Cell activation ; Circadian rhythm ; Estrogens ; Genes ; Glial cells ; Heat shock proteins ; Humans ; Hydrocarbons ; Hypothalamus ; Inflammation ; Kinases ; Ligands ; Metabolism ; Metabolites ; Microbiota ; Mitochondria ; Nervous system ; Neurodegenerative diseases ; Neurogenesis ; Oxidative stress ; Pathology ; Phenotypes ; Physiology ; Receptors, Aryl Hydrocarbon - metabolism ; Review ; Senescence ; Signal Transduction</subject><ispartof>Cells (Basel, Switzerland), 2021-10, Vol.10 (10), p.2729</ispartof><rights>2021 by the authors. 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/). 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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. 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Tischkau, Shelley A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-290d4b2b6db3af46962e00e96b133250c5f3c69d9416349b31005325d5e97a1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aging</topic><topic>Aging - metabolism</topic><topic>AhR endogenous/exogenous ligands</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>aryl hydrocarbon receptor</topic><topic>Biosensors</topic><topic>Blood-brain barrier</topic><topic>Brain - metabolism</topic><topic>brain aging hallmarks</topic><topic>Brain diseases</topic><topic>Brain Diseases - metabolism</topic><topic>Brain Diseases - pathology</topic><topic>Cell activation</topic><topic>Circadian rhythm</topic><topic>Estrogens</topic><topic>Genes</topic><topic>Glial cells</topic><topic>Heat shock proteins</topic><topic>Humans</topic><topic>Hydrocarbons</topic><topic>Hypothalamus</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Microbiota</topic><topic>Mitochondria</topic><topic>Nervous system</topic><topic>Neurodegenerative diseases</topic><topic>Neurogenesis</topic><topic>Oxidative stress</topic><topic>Pathology</topic><topic>Phenotypes</topic><topic>Physiology</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>Review</topic><topic>Senescence</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ojo, Emmanuel S</creatorcontrib><creatorcontrib>Tischkau, Shelley A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Biological Sciences</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Cells (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ojo, Emmanuel S</au><au>Tischkau, Shelley A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe</atitle><jtitle>Cells (Basel, Switzerland)</jtitle><addtitle>Cells</addtitle><date>2021-10-13</date><risdate>2021</risdate><volume>10</volume><issue>10</issue><spage>2729</spage><pages>2729-</pages><issn>2073-4409</issn><eissn>2073-4409</eissn><abstract>In recent years, aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered to be involved in aging phenotypes across several species. 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subjects | Aging Aging - metabolism AhR endogenous/exogenous ligands Alzheimer's disease Animals aryl hydrocarbon receptor Biosensors Blood-brain barrier Brain - metabolism brain aging hallmarks Brain diseases Brain Diseases - metabolism Brain Diseases - pathology Cell activation Circadian rhythm Estrogens Genes Glial cells Heat shock proteins Humans Hydrocarbons Hypothalamus Inflammation Kinases Ligands Metabolism Metabolites Microbiota Mitochondria Nervous system Neurodegenerative diseases Neurogenesis Oxidative stress Pathology Phenotypes Physiology Receptors, Aryl Hydrocarbon - metabolism Review Senescence Signal Transduction |
title | The Role of AhR in the Hallmarks of Brain Aging: Friend and Foe |
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