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The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?

It has been postulated for some time that endogenous digitalis-like substances, also called cardiotonic steroids (CTS), exist, and that these substances are involved in sodium handling. Within the past 20 years, these substances have been unequivocally identified and measurements of circulating and...

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Detalles Bibliográficos
Autores principales: Xie, Joe X., Shapiro, Anna Pearl, Shapiro, Joseph Isaac
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101451/
https://www.ncbi.nlm.nih.gov/pubmed/25101054
http://dx.doi.org/10.3389/fendo.2014.00097
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author Xie, Joe X.
Shapiro, Anna Pearl
Shapiro, Joseph Isaac
author_facet Xie, Joe X.
Shapiro, Anna Pearl
Shapiro, Joseph Isaac
author_sort Xie, Joe X.
collection PubMed
description It has been postulated for some time that endogenous digitalis-like substances, also called cardiotonic steroids (CTS), exist, and that these substances are involved in sodium handling. Within the past 20 years, these substances have been unequivocally identified and measurements of circulating and tissue concentrations have been made. More recently, it has been identified that CTS also mediate signal transduction through the Na/K-ATPase, and consequently been implicated in profibrotic pathways. This review will discuss the mechanism of CTS in renal sodium handling and a potential “trade-off” effect from their role in inducing tissue fibrosis.
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spelling pubmed-41014512014-08-06 The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling? Xie, Joe X. Shapiro, Anna Pearl Shapiro, Joseph Isaac Front Endocrinol (Lausanne) Endocrinology It has been postulated for some time that endogenous digitalis-like substances, also called cardiotonic steroids (CTS), exist, and that these substances are involved in sodium handling. Within the past 20 years, these substances have been unequivocally identified and measurements of circulating and tissue concentrations have been made. More recently, it has been identified that CTS also mediate signal transduction through the Na/K-ATPase, and consequently been implicated in profibrotic pathways. This review will discuss the mechanism of CTS in renal sodium handling and a potential “trade-off” effect from their role in inducing tissue fibrosis. Frontiers Media S.A. 2014-07-17 /pmc/articles/PMC4101451/ /pubmed/25101054 http://dx.doi.org/10.3389/fendo.2014.00097 Text en Copyright © 2014 Xie, Shapiro and Shapiro. 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
Xie, Joe X.
Shapiro, Anna Pearl
Shapiro, Joseph Isaac
The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?
title The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?
title_full The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?
title_fullStr The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?
title_full_unstemmed The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?
title_short The Trade-Off between Dietary Salt and Cardiovascular Disease; A Role for Na/K-ATPase Signaling?
title_sort trade-off between dietary salt and cardiovascular disease; a role for na/k-atpase signaling?
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101451/
https://www.ncbi.nlm.nih.gov/pubmed/25101054
http://dx.doi.org/10.3389/fendo.2014.00097
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