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A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.
't Hart, Daan C; van der Vlag, Johan; Nijenhuis, Tom.
Afiliação
  • 't Hart DC; Department of Nephrology, Radboud Research Institute for Medical Innovation, Radboud University Medical Centre, 6500 HB Nijmegen, The Netherlands.
  • van der Vlag J; Department of Nephrology, Radboud Research Institute for Medical Innovation, Radboud University Medical Centre, 6500 HB Nijmegen, The Netherlands.
  • Nijenhuis T; Department of Nephrology, Radboud Research Institute for Medical Innovation, Radboud University Medical Centre, 6500 HB Nijmegen, The Netherlands.
Int J Mol Sci ; 24(22)2023 Nov 16.
Article em En | MEDLINE | ID: mdl-38003608
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 Ca2+-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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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Podócitos / Nefropatias Limite: Humans Idioma: En Revista: Int J Mol Sci Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Podócitos / Nefropatias Limite: Humans Idioma: En Revista: Int J Mol Sci Ano de publicação: 2023 Tipo de documento: Article