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A Putative Role for TRPC6 in Immune-Mediated Kidney Injury

Excessive activation of the immune system is the cause of a wide variety of renal diseases. However, the pathogenic mechanisms underlying the aberrant activation of the immune system in the kidneys often remain unknown. TRPC6, a member of the Ca(2+)-permeant family of TRPC channels, is important in...

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Detalles Bibliográficos
Autores principales: ‘t Hart, Daan C., van der Vlag, Johan, Nijenhuis, Tom
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10671681/
https://www.ncbi.nlm.nih.gov/pubmed/38003608
http://dx.doi.org/10.3390/ijms242216419
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author ‘t Hart, Daan C.
van der Vlag, Johan
Nijenhuis, Tom
author_facet ‘t Hart, Daan C.
van der Vlag, Johan
Nijenhuis, Tom
author_sort ‘t Hart, Daan C.
collection PubMed
description Excessive activation of the immune system is the cause of a wide variety of renal diseases. However, the pathogenic mechanisms underlying the aberrant activation of the immune system in the kidneys often remain unknown. TRPC6, a member of the Ca(2+)-permeant family of TRPC channels, is important in glomerular epithelial cells or podocytes for the process of glomerular filtration. In addition, TRPC6 plays a crucial role in the development of kidney injuries by inducing podocyte injury. However, an increasing number of studies suggest that TRPC6 is also responsible for tightly regulating the immune cell functions. It remains elusive whether the role of TRPC6 in the immune system and the pathogenesis of renal inflammation are intertwined. In this review, we present an overview of the current knowledge of how TRPC6 coordinates the immune cell functions and propose the hypothesis that TRPC6 might play a pivotal role in the development of kidney injury via its role in the immune system.
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spelling pubmed-106716812023-11-16 A Putative Role for TRPC6 in Immune-Mediated Kidney Injury ‘t Hart, Daan C. van der Vlag, Johan Nijenhuis, Tom Int J Mol Sci Review Excessive activation of the immune system is the cause of a wide variety of renal diseases. However, the pathogenic mechanisms underlying the aberrant activation of the immune system in the kidneys often remain unknown. TRPC6, a member of the Ca(2+)-permeant family of TRPC channels, is important in glomerular epithelial cells or podocytes for the process of glomerular filtration. In addition, TRPC6 plays a crucial role in the development of kidney injuries by inducing podocyte injury. However, an increasing number of studies suggest that TRPC6 is also responsible for tightly regulating the immune cell functions. It remains elusive whether the role of TRPC6 in the immune system and the pathogenesis of renal inflammation are intertwined. In this review, we present an overview of the current knowledge of how TRPC6 coordinates the immune cell functions and propose the hypothesis that TRPC6 might play a pivotal role in the development of kidney injury via its role in the immune system. MDPI 2023-11-16 /pmc/articles/PMC10671681/ /pubmed/38003608 http://dx.doi.org/10.3390/ijms242216419 Text en © 2023 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
‘t Hart, Daan C.
van der Vlag, Johan
Nijenhuis, Tom
A Putative Role for TRPC6 in Immune-Mediated Kidney Injury
title A Putative Role for TRPC6 in Immune-Mediated Kidney Injury
title_full A Putative Role for TRPC6 in Immune-Mediated Kidney Injury
title_fullStr A Putative Role for TRPC6 in Immune-Mediated Kidney Injury
title_full_unstemmed A Putative Role for TRPC6 in Immune-Mediated Kidney Injury
title_short A Putative Role for TRPC6 in Immune-Mediated Kidney Injury
title_sort putative role for trpc6 in immune-mediated kidney injury
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10671681/
https://www.ncbi.nlm.nih.gov/pubmed/38003608
http://dx.doi.org/10.3390/ijms242216419
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