Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism

Mutations in the chloride channel ClC-2 have been found in primary aldosteronism (PA). Here, Göppner et al. generate transgenic mice expressing a mutant form of ClC-2 that displays increased chloride currents like patient mutations, and find it recapitulates the key pathological features of PA.

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Autores principales:	Corinna Göppner, Ian J. Orozco, Maja B. Hoegg-Beiler, Audrey H. Soria, Christian A. Hübner, Fabio L. Fernandes-Rosa, Sheerazed Boulkroun, Maria-Christina Zennaro, Thomas J. Jentsch
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/84c646bd88094254bc90a68de9c28af6
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spelling	oai:doaj.org-article:84c646bd88094254bc90a68de9c28af62021-12-02T17:01:45ZPathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism10.1038/s41467-019-12113-92041-1723https://doaj.org/article/84c646bd88094254bc90a68de9c28af62019-10-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-12113-9https://doaj.org/toc/2041-1723Mutations in the chloride channel ClC-2 have been found in primary aldosteronism (PA). Here, Göppner et al. generate transgenic mice expressing a mutant form of ClC-2 that displays increased chloride currents like patient mutations, and find it recapitulates the key pathological features of PA.Corinna GöppnerIan J. OrozcoMaja B. Hoegg-BeilerAudrey H. SoriaChristian A. HübnerFabio L. Fernandes-RosaSheerazed BoulkrounMaria-Christina ZennaroThomas J. JentschNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-13 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Corinna Göppner Ian J. Orozco Maja B. Hoegg-Beiler Audrey H. Soria Christian A. Hübner Fabio L. Fernandes-Rosa Sheerazed Boulkroun Maria-Christina Zennaro Thomas J. Jentsch Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism
description	Mutations in the chloride channel ClC-2 have been found in primary aldosteronism (PA). Here, Göppner et al. generate transgenic mice expressing a mutant form of ClC-2 that displays increased chloride currents like patient mutations, and find it recapitulates the key pathological features of PA.
format	article
author	Corinna Göppner Ian J. Orozco Maja B. Hoegg-Beiler Audrey H. Soria Christian A. Hübner Fabio L. Fernandes-Rosa Sheerazed Boulkroun Maria-Christina Zennaro Thomas J. Jentsch
author_facet	Corinna Göppner Ian J. Orozco Maja B. Hoegg-Beiler Audrey H. Soria Christian A. Hübner Fabio L. Fernandes-Rosa Sheerazed Boulkroun Maria-Christina Zennaro Thomas J. Jentsch
author_sort	Corinna Göppner
title	Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism
title_short	Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism
title_full	Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism
title_fullStr	Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism
title_full_unstemmed	Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism
title_sort	pathogenesis of hypertension in a mouse model for human clcn2 related hyperaldosteronism
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/84c646bd88094254bc90a68de9c28af6
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Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism

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