Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases
The endogenous ouabain (EO) is a steroid hormone secreted by the adrenal gland with cardio-tonic effects. In this article, we have reviewed and summarized the most recent reports about EO, particularly with regard to how it may interact with specific genetic backgrounds. We have focused our attentio...
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doaj-1300f07b8728464cbf1b55fb4640d83a2020-11-24T23:01:25ZengMDPI AGInternational Journal of Molecular Sciences1422-00672018-07-01197194810.3390/ijms19071948ijms19071948Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal DiseasesMarco Simonini0Paola Casanova1Lorena Citterio2Elisabetta Messaggio3Chiara Lanzani4Paolo Manunta5Genomics of Renal Disease and Hypertension Unit, IRCCS San Raffaele Scientific Institute, Università Vita Salute San Raffaele, 20132 Milan, ItalyGenomics of Renal Disease and Hypertension Unit, IRCCS San Raffaele Scientific Institute, Università Vita Salute San Raffaele, 20132 Milan, ItalyGenomics of Renal Disease and Hypertension Unit, IRCCS San Raffaele Scientific Institute, Università Vita Salute San Raffaele, 20132 Milan, ItalyGenomics of Renal Disease and Hypertension Unit, IRCCS San Raffaele Scientific Institute, Università Vita Salute San Raffaele, 20132 Milan, ItalyGenomics of Renal Disease and Hypertension Unit, IRCCS San Raffaele Scientific Institute, Università Vita Salute San Raffaele, 20132 Milan, ItalyGenomics of Renal Disease and Hypertension Unit, IRCCS San Raffaele Scientific Institute, Università Vita Salute San Raffaele, 20132 Milan, ItalyThe endogenous ouabain (EO) is a steroid hormone secreted by the adrenal gland with cardio-tonic effects. In this article, we have reviewed and summarized the most recent reports about EO, particularly with regard to how it may interact with specific genetic backgrounds. We have focused our attention on the EO’s potential pathogenic role in several diseases, including renal failure, essential hypertension and heart failure. Notably, these reports have demonstrated that EO acts as a pro-hypertrophic and growth-promoting hormone, which might lead to a cardiac remodeling affecting cardiovascular functions and structures. In addition, a possible role of EO in the development of acute kidney injury has been hypothesized. During the last decays, many important improvements permitted a deeper understanding of EO’s metabolisms and functions, including the characteristics of its receptor and the effects of its activation. Such progresses indicated that EO has significant implications in the pathogenesis of many common diseases. The patho-physiological role of EO in the development of hypertension and other cardiac and renal complications have laid the basis for the development of a new selective compound that could selectively modulate the genetic and molecular mechanisms involved in EO’s action. It is evident that the knowledge of EO has incredibly increased; however, many important areas remain to be further investigated.http://www.mdpi.com/1422-0067/19/7/1948cardio-tonic steroidsendogenous ouabainadducinhypertensionrenal damage |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Marco Simonini Paola Casanova Lorena Citterio Elisabetta Messaggio Chiara Lanzani Paolo Manunta |
spellingShingle |
Marco Simonini Paola Casanova Lorena Citterio Elisabetta Messaggio Chiara Lanzani Paolo Manunta Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases International Journal of Molecular Sciences cardio-tonic steroids endogenous ouabain adducin hypertension renal damage |
author_facet |
Marco Simonini Paola Casanova Lorena Citterio Elisabetta Messaggio Chiara Lanzani Paolo Manunta |
author_sort |
Marco Simonini |
title |
Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases |
title_short |
Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases |
title_full |
Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases |
title_fullStr |
Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases |
title_full_unstemmed |
Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases |
title_sort |
endogenous ouabain and related genes in the translation from hypertension to renal diseases |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1422-0067 |
publishDate |
2018-07-01 |
description |
The endogenous ouabain (EO) is a steroid hormone secreted by the adrenal gland with cardio-tonic effects. In this article, we have reviewed and summarized the most recent reports about EO, particularly with regard to how it may interact with specific genetic backgrounds. We have focused our attention on the EO’s potential pathogenic role in several diseases, including renal failure, essential hypertension and heart failure. Notably, these reports have demonstrated that EO acts as a pro-hypertrophic and growth-promoting hormone, which might lead to a cardiac remodeling affecting cardiovascular functions and structures. In addition, a possible role of EO in the development of acute kidney injury has been hypothesized. During the last decays, many important improvements permitted a deeper understanding of EO’s metabolisms and functions, including the characteristics of its receptor and the effects of its activation. Such progresses indicated that EO has significant implications in the pathogenesis of many common diseases. The patho-physiological role of EO in the development of hypertension and other cardiac and renal complications have laid the basis for the development of a new selective compound that could selectively modulate the genetic and molecular mechanisms involved in EO’s action. It is evident that the knowledge of EO has incredibly increased; however, many important areas remain to be further investigated. |
topic |
cardio-tonic steroids endogenous ouabain adducin hypertension renal damage |
url |
http://www.mdpi.com/1422-0067/19/7/1948 |
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