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Role of TRPA1 in Tissue Damage and Kidney Disease

TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or...

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Autores principales: Wu, Chung-Kuan, Lin, Ji-Fan, Lee, Tzong-Shyuan, Kou, Yu Ru, Tarng, Der-Cherng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8036557/
https://www.ncbi.nlm.nih.gov/pubmed/33810314
http://dx.doi.org/10.3390/ijms22073415
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author Wu, Chung-Kuan
Lin, Ji-Fan
Lee, Tzong-Shyuan
Kou, Yu Ru
Tarng, Der-Cherng
author_facet Wu, Chung-Kuan
Lin, Ji-Fan
Lee, Tzong-Shyuan
Kou, Yu Ru
Tarng, Der-Cherng
author_sort Wu, Chung-Kuan
collection PubMed
description TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or endogenous irritants in the injured tissue. However, chronic inflammation after repeated noxious stimuli may result in the development of several diseases. In addition to sensory neurons, TRPA1, activated by inflammatory agents from some non-neuronal cells in the injured area or disease, might promote or protect disease progression. Therefore, TRPA1 works as a molecular sentinel of tissue damage or as an inflammation gatekeeper. Most kidney damage cases are associated with inflammation. In this review, we summarised the role of TRPA1 in neurogenic or non-neurogenic inflammation and in kidney disease, especially the non-neuronal TRPA1. In in vivo animal studies, TRPA1 prevented sepsis-induced or Ang-II-induced and ischemia-reperfusion renal injury by maintaining mitochondrial haemostasis or via the downregulation of macrophage-mediated inflammation, respectively. Renal tubular epithelial TRPA1 acts as an oxidative stress sensor to mediate hypoxia–reoxygenation injury in vitro and ischaemia–reperfusion-induced kidney injury in vivo through MAPKs/NF-kB signalling. Acute kidney injury (AKI) patients with high renal tubular TRPA1 expression had low complete renal function recovery. In renal disease, TPRA1 plays different roles in different cell types accordingly. These findings depict the important role of TRPA1 and warrant further investigation.
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spelling pubmed-80365572021-04-12 Role of TRPA1 in Tissue Damage and Kidney Disease Wu, Chung-Kuan Lin, Ji-Fan Lee, Tzong-Shyuan Kou, Yu Ru Tarng, Der-Cherng Int J Mol Sci Review TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or endogenous irritants in the injured tissue. However, chronic inflammation after repeated noxious stimuli may result in the development of several diseases. In addition to sensory neurons, TRPA1, activated by inflammatory agents from some non-neuronal cells in the injured area or disease, might promote or protect disease progression. Therefore, TRPA1 works as a molecular sentinel of tissue damage or as an inflammation gatekeeper. Most kidney damage cases are associated with inflammation. In this review, we summarised the role of TRPA1 in neurogenic or non-neurogenic inflammation and in kidney disease, especially the non-neuronal TRPA1. In in vivo animal studies, TRPA1 prevented sepsis-induced or Ang-II-induced and ischemia-reperfusion renal injury by maintaining mitochondrial haemostasis or via the downregulation of macrophage-mediated inflammation, respectively. Renal tubular epithelial TRPA1 acts as an oxidative stress sensor to mediate hypoxia–reoxygenation injury in vitro and ischaemia–reperfusion-induced kidney injury in vivo through MAPKs/NF-kB signalling. Acute kidney injury (AKI) patients with high renal tubular TRPA1 expression had low complete renal function recovery. In renal disease, TPRA1 plays different roles in different cell types accordingly. These findings depict the important role of TRPA1 and warrant further investigation. MDPI 2021-03-26 /pmc/articles/PMC8036557/ /pubmed/33810314 http://dx.doi.org/10.3390/ijms22073415 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 (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Review
Wu, Chung-Kuan
Lin, Ji-Fan
Lee, Tzong-Shyuan
Kou, Yu Ru
Tarng, Der-Cherng
Role of TRPA1 in Tissue Damage and Kidney Disease
title Role of TRPA1 in Tissue Damage and Kidney Disease
title_full Role of TRPA1 in Tissue Damage and Kidney Disease
title_fullStr Role of TRPA1 in Tissue Damage and Kidney Disease
title_full_unstemmed Role of TRPA1 in Tissue Damage and Kidney Disease
title_short Role of TRPA1 in Tissue Damage and Kidney Disease
title_sort role of trpa1 in tissue damage and kidney disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8036557/
https://www.ncbi.nlm.nih.gov/pubmed/33810314
http://dx.doi.org/10.3390/ijms22073415
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