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Autophagy and the (Pro)renin Receptor
The (pro)renin receptor (PRR) is a newly reported member of the renin-angiotensin system (RAS); a hormonal cascade responsible for regulating blood pressure. Originally, identification of PRR was heralded as the next drug target of the RAS, of which such therapies would have increased benefits again...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2013
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800846/ https://www.ncbi.nlm.nih.gov/pubmed/24155743 http://dx.doi.org/10.3389/fendo.2013.00155 |
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author | Binger, Katrina J. Muller, Dominik N. |
author_facet | Binger, Katrina J. Muller, Dominik N. |
author_sort | Binger, Katrina J. |
collection | PubMed |
description | The (pro)renin receptor (PRR) is a newly reported member of the renin-angiotensin system (RAS); a hormonal cascade responsible for regulating blood pressure. Originally, identification of PRR was heralded as the next drug target of the RAS, of which such therapies would have increased benefits against target-organ damage and hypertension. However, in the years since its discovery, several conditional knockout mouse models of PRR have demonstrated an essential role for this receptor unrelated to the RAS and blood pressure. Specific deletion of PRR in podocytes or cardiomyocytes resulted in the rapid onset of organ failure and subsequently animal mortality after only a matter of weeks. In both cell types, loss of PRR resulted in the intracellular accumulation of autophagosomes and misfolded proteins, indicating a disturbance in autophagy. In light of the fact that the majority of PRR is located intracellularly, this molecular function appears to be more relevant than its ability to bind to high, non-physiological concentrations of (pro)renin. This review will focus on the role of PRR in autophagy and its importance in maintaining cellular homeostasis. Understanding the link between PRR, autophagy and how its loss results in cell death will be essential for deciphering its role in physiology and pathology. |
format | Online Article Text |
id | pubmed-3800846 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-38008462013-10-23 Autophagy and the (Pro)renin Receptor Binger, Katrina J. Muller, Dominik N. Front Endocrinol (Lausanne) Endocrinology The (pro)renin receptor (PRR) is a newly reported member of the renin-angiotensin system (RAS); a hormonal cascade responsible for regulating blood pressure. Originally, identification of PRR was heralded as the next drug target of the RAS, of which such therapies would have increased benefits against target-organ damage and hypertension. However, in the years since its discovery, several conditional knockout mouse models of PRR have demonstrated an essential role for this receptor unrelated to the RAS and blood pressure. Specific deletion of PRR in podocytes or cardiomyocytes resulted in the rapid onset of organ failure and subsequently animal mortality after only a matter of weeks. In both cell types, loss of PRR resulted in the intracellular accumulation of autophagosomes and misfolded proteins, indicating a disturbance in autophagy. In light of the fact that the majority of PRR is located intracellularly, this molecular function appears to be more relevant than its ability to bind to high, non-physiological concentrations of (pro)renin. This review will focus on the role of PRR in autophagy and its importance in maintaining cellular homeostasis. Understanding the link between PRR, autophagy and how its loss results in cell death will be essential for deciphering its role in physiology and pathology. Frontiers Media S.A. 2013-10-21 /pmc/articles/PMC3800846/ /pubmed/24155743 http://dx.doi.org/10.3389/fendo.2013.00155 Text en Copyright © 2013 Binger and Muller. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Endocrinology Binger, Katrina J. Muller, Dominik N. Autophagy and the (Pro)renin Receptor |
title | Autophagy and the (Pro)renin Receptor |
title_full | Autophagy and the (Pro)renin Receptor |
title_fullStr | Autophagy and the (Pro)renin Receptor |
title_full_unstemmed | Autophagy and the (Pro)renin Receptor |
title_short | Autophagy and the (Pro)renin Receptor |
title_sort | autophagy and the (pro)renin receptor |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800846/ https://www.ncbi.nlm.nih.gov/pubmed/24155743 http://dx.doi.org/10.3389/fendo.2013.00155 |
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