The Pathological Role of Pro(Renin) Receptor in Renal Inflammation

(Pro)renin receptor (PRR) is the recently discovered component of the renin-angiotensin-aldosterone system (RAS). Many organs contain their own RAS, wherein PRR can exert organ-specific localized effects. The Binding of prorenin/renin to PRR activates angiotensin-dependent and independent pathways w...

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Autores principales: Quadri, Syed S, Cooper, Caleb, Ghaffar, Dawood, Vaishnav, Hitesh, Nahar, Ludmila
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2021
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7989955/
https://www.ncbi.nlm.nih.gov/pubmed/33776491
http://dx.doi.org/10.2147/JEP.S297682
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author Quadri, Syed S
Cooper, Caleb
Ghaffar, Dawood
Vaishnav, Hitesh
Nahar, Ludmila
author_facet Quadri, Syed S
Cooper, Caleb
Ghaffar, Dawood
Vaishnav, Hitesh
Nahar, Ludmila
author_sort Quadri, Syed S
collection PubMed
description (Pro)renin receptor (PRR) is the recently discovered component of the renin-angiotensin-aldosterone system (RAS). Many organs contain their own RAS, wherein PRR can exert organ-specific localized effects. The Binding of prorenin/renin to PRR activates angiotensin-dependent and independent pathways which leads to the development of physiological and pathological effects. Continued progress in PRR research suggests that the upregulation of PRR contributes to the development of hypertension, glomerular injury, and progression of kidney disease and inflammation. In the current review, we highlight the function of the PRR in renal inflammation in pathophysiological conditions.
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spelling pubmed-79899552021-03-25 The Pathological Role of Pro(Renin) Receptor in Renal Inflammation Quadri, Syed S Cooper, Caleb Ghaffar, Dawood Vaishnav, Hitesh Nahar, Ludmila J Exp Pharmacol Review (Pro)renin receptor (PRR) is the recently discovered component of the renin-angiotensin-aldosterone system (RAS). Many organs contain their own RAS, wherein PRR can exert organ-specific localized effects. The Binding of prorenin/renin to PRR activates angiotensin-dependent and independent pathways which leads to the development of physiological and pathological effects. Continued progress in PRR research suggests that the upregulation of PRR contributes to the development of hypertension, glomerular injury, and progression of kidney disease and inflammation. In the current review, we highlight the function of the PRR in renal inflammation in pathophysiological conditions. Dove 2021-03-19 /pmc/articles/PMC7989955/ /pubmed/33776491 http://dx.doi.org/10.2147/JEP.S297682 Text en © 2021 Quadri et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Review
Quadri, Syed S
Cooper, Caleb
Ghaffar, Dawood
Vaishnav, Hitesh
Nahar, Ludmila
The Pathological Role of Pro(Renin) Receptor in Renal Inflammation
title The Pathological Role of Pro(Renin) Receptor in Renal Inflammation
title_full The Pathological Role of Pro(Renin) Receptor in Renal Inflammation
title_fullStr The Pathological Role of Pro(Renin) Receptor in Renal Inflammation
title_full_unstemmed The Pathological Role of Pro(Renin) Receptor in Renal Inflammation
title_short The Pathological Role of Pro(Renin) Receptor in Renal Inflammation
title_sort pathological role of pro(renin) receptor in renal inflammation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7989955/
https://www.ncbi.nlm.nih.gov/pubmed/33776491
http://dx.doi.org/10.2147/JEP.S297682
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