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Juxtaglomerular Cell Phenotypic Plasticity

Renin is the first and rate-limiting step of the renin-angiotensin system. The exclusive source of renin in the circulation are the juxtaglomerular cells of the kidney, which line the afferent arterioles at the entrance of the glomeruli. Normally, renin production by these cells suffices to maintain...

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Detalles Bibliográficos
Autores principales: Martini, Alexandre Góes, Danser, A. H. Jan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5574949/
https://www.ncbi.nlm.nih.gov/pubmed/28527017
http://dx.doi.org/10.1007/s40292-017-0212-5
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author Martini, Alexandre Góes
Danser, A. H. Jan
author_facet Martini, Alexandre Góes
Danser, A. H. Jan
author_sort Martini, Alexandre Góes
collection PubMed
description Renin is the first and rate-limiting step of the renin-angiotensin system. The exclusive source of renin in the circulation are the juxtaglomerular cells of the kidney, which line the afferent arterioles at the entrance of the glomeruli. Normally, renin production by these cells suffices to maintain homeostasis. However, under chronic stimulation of renin release, for instance during a low-salt diet or antihypertensive therapy, cells that previously expressed renin during congenital life re-convert to a renin-producing cell phenotype, a phenomenon which is known as “recruitment”. How exactly such differentiation occurs remains to be clarified. This review critically discusses the phenotypic plasticity of renin cells, connecting them not only to the classical concept of blood pressure regulation, but also to more complex contexts such as development and growth processes, cell repair mechanisms and tissue regeneration.
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spelling pubmed-55749492017-09-18 Juxtaglomerular Cell Phenotypic Plasticity Martini, Alexandre Góes Danser, A. H. Jan High Blood Press Cardiovasc Prev Review Article Renin is the first and rate-limiting step of the renin-angiotensin system. The exclusive source of renin in the circulation are the juxtaglomerular cells of the kidney, which line the afferent arterioles at the entrance of the glomeruli. Normally, renin production by these cells suffices to maintain homeostasis. However, under chronic stimulation of renin release, for instance during a low-salt diet or antihypertensive therapy, cells that previously expressed renin during congenital life re-convert to a renin-producing cell phenotype, a phenomenon which is known as “recruitment”. How exactly such differentiation occurs remains to be clarified. This review critically discusses the phenotypic plasticity of renin cells, connecting them not only to the classical concept of blood pressure regulation, but also to more complex contexts such as development and growth processes, cell repair mechanisms and tissue regeneration. Springer International Publishing 2017-05-19 2017 /pmc/articles/PMC5574949/ /pubmed/28527017 http://dx.doi.org/10.1007/s40292-017-0212-5 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review Article
Martini, Alexandre Góes
Danser, A. H. Jan
Juxtaglomerular Cell Phenotypic Plasticity
title Juxtaglomerular Cell Phenotypic Plasticity
title_full Juxtaglomerular Cell Phenotypic Plasticity
title_fullStr Juxtaglomerular Cell Phenotypic Plasticity
title_full_unstemmed Juxtaglomerular Cell Phenotypic Plasticity
title_short Juxtaglomerular Cell Phenotypic Plasticity
title_sort juxtaglomerular cell phenotypic plasticity
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5574949/
https://www.ncbi.nlm.nih.gov/pubmed/28527017
http://dx.doi.org/10.1007/s40292-017-0212-5
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