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Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis

Arrhythmogenic cardiomyopathy (ACM) is a genetic cardiac condition characterized by the replacement of the ventricular myocardium with fibro-fatty tissue, by arrhythmias and sudden death. Adipogenesis in ACM is considered an aberrant remodeling following myocardial loss. Which cell type(s) is (are)...

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Autores principales: Stadiotti, Ilaria, Catto, Valentina, Casella, Michela, Tondo, Claudio, Pompilio, Giulio, Sommariva, Elena
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5722955/
https://www.ncbi.nlm.nih.gov/pubmed/28983804
http://dx.doi.org/10.1007/s12265-017-9767-8
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author Stadiotti, Ilaria
Catto, Valentina
Casella, Michela
Tondo, Claudio
Pompilio, Giulio
Sommariva, Elena
author_facet Stadiotti, Ilaria
Catto, Valentina
Casella, Michela
Tondo, Claudio
Pompilio, Giulio
Sommariva, Elena
author_sort Stadiotti, Ilaria
collection PubMed
description Arrhythmogenic cardiomyopathy (ACM) is a genetic cardiac condition characterized by the replacement of the ventricular myocardium with fibro-fatty tissue, by arrhythmias and sudden death. Adipogenesis in ACM is considered an aberrant remodeling following myocardial loss. Which cell type(s) is (are) responsible for the adipose replacement is still matter of debate. A systematic overview of the different cells that have been, over time, considered as main players in adipose replacement is provided. The comprehension of the cellular component giving rise to arrhythmogenic cardiomyopathy substrate defects may represent both an essential tool for mechanistic studies of disease pathogenesis and a novel possible therapeutic target.
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spelling pubmed-57229552017-12-12 Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis Stadiotti, Ilaria Catto, Valentina Casella, Michela Tondo, Claudio Pompilio, Giulio Sommariva, Elena J Cardiovasc Transl Res Review Arrhythmogenic cardiomyopathy (ACM) is a genetic cardiac condition characterized by the replacement of the ventricular myocardium with fibro-fatty tissue, by arrhythmias and sudden death. Adipogenesis in ACM is considered an aberrant remodeling following myocardial loss. Which cell type(s) is (are) responsible for the adipose replacement is still matter of debate. A systematic overview of the different cells that have been, over time, considered as main players in adipose replacement is provided. The comprehension of the cellular component giving rise to arrhythmogenic cardiomyopathy substrate defects may represent both an essential tool for mechanistic studies of disease pathogenesis and a novel possible therapeutic target. Springer US 2017-10-05 2017 /pmc/articles/PMC5722955/ /pubmed/28983804 http://dx.doi.org/10.1007/s12265-017-9767-8 Text en © The Author(s). This article is an open access publication 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Stadiotti, Ilaria
Catto, Valentina
Casella, Michela
Tondo, Claudio
Pompilio, Giulio
Sommariva, Elena
Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis
title Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis
title_full Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis
title_fullStr Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis
title_full_unstemmed Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis
title_short Arrhythmogenic Cardiomyopathy: the Guilty Party in Adipogenesis
title_sort arrhythmogenic cardiomyopathy: the guilty party in adipogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5722955/
https://www.ncbi.nlm.nih.gov/pubmed/28983804
http://dx.doi.org/10.1007/s12265-017-9767-8
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