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Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease

The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor that binds diverse endogenous and xenobiotic ligands, which regulate AHR stability, transcriptional activity, and cell signaling. AHR activity is strongly implicated throughout the course of chronic kidney disease (...

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Detalles Bibliográficos
Autores principales: Curran, Colleen S., Kopp, Jeffrey B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8882872/
https://www.ncbi.nlm.nih.gov/pubmed/35237156
http://dx.doi.org/10.3389/fphar.2022.782199
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author Curran, Colleen S.
Kopp, Jeffrey B.
author_facet Curran, Colleen S.
Kopp, Jeffrey B.
author_sort Curran, Colleen S.
collection PubMed
description The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor that binds diverse endogenous and xenobiotic ligands, which regulate AHR stability, transcriptional activity, and cell signaling. AHR activity is strongly implicated throughout the course of chronic kidney disease (CKD). Many diverse organic molecules bind and activate AHR and these ligands are reported to either promote glomerular and tubular damage or protect against kidney injury. AHR crosstalk with estrogen, peroxisome proliferator-activated receptor-γ, and NF-κB pathways may contribute to the diversity of AHR responses during the various forms and stages of CKD. The roles of AHR in kidney fibrosis, metabolism and the renin angiotensin system are described to offer insight into CKD pathogenesis and therapies.
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spelling pubmed-88828722022-03-01 Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease Curran, Colleen S. Kopp, Jeffrey B. Front Pharmacol Pharmacology The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor that binds diverse endogenous and xenobiotic ligands, which regulate AHR stability, transcriptional activity, and cell signaling. AHR activity is strongly implicated throughout the course of chronic kidney disease (CKD). Many diverse organic molecules bind and activate AHR and these ligands are reported to either promote glomerular and tubular damage or protect against kidney injury. AHR crosstalk with estrogen, peroxisome proliferator-activated receptor-γ, and NF-κB pathways may contribute to the diversity of AHR responses during the various forms and stages of CKD. The roles of AHR in kidney fibrosis, metabolism and the renin angiotensin system are described to offer insight into CKD pathogenesis and therapies. Frontiers Media S.A. 2022-02-14 /pmc/articles/PMC8882872/ /pubmed/35237156 http://dx.doi.org/10.3389/fphar.2022.782199 Text en Copyright © 2022 Curran and Kopp. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Curran, Colleen S.
Kopp, Jeffrey B.
Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease
title Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease
title_full Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease
title_fullStr Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease
title_full_unstemmed Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease
title_short Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease
title_sort aryl hydrocarbon receptor mechanisms affecting chronic kidney disease
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8882872/
https://www.ncbi.nlm.nih.gov/pubmed/35237156
http://dx.doi.org/10.3389/fphar.2022.782199
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