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Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinica...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483129/ https://www.ncbi.nlm.nih.gov/pubmed/23109667 http://dx.doi.org/10.1083/jcb.201207033 |
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author | Teekakirikul, Polakit Padera, Robert F. Seidman, J.G. Seidman, Christine E. |
author_facet | Teekakirikul, Polakit Padera, Robert F. Seidman, J.G. Seidman, Christine E. |
author_sort | Teekakirikul, Polakit |
collection | PubMed |
description | Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinical manifestations of disease. Studies in these models have provided unexpected insights into the biophysical and biochemical properties of mutated contractile proteins and may help to improve clinical diagnosis and management of patients with HCM. |
format | Online Article Text |
id | pubmed-3483129 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-34831292013-04-29 Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics Teekakirikul, Polakit Padera, Robert F. Seidman, J.G. Seidman, Christine E. J Cell Biol News Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinical manifestations of disease. Studies in these models have provided unexpected insights into the biophysical and biochemical properties of mutated contractile proteins and may help to improve clinical diagnosis and management of patients with HCM. The Rockefeller University Press 2012-10-29 /pmc/articles/PMC3483129/ /pubmed/23109667 http://dx.doi.org/10.1083/jcb.201207033 Text en © 2012 Teekakirikul et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | News Teekakirikul, Polakit Padera, Robert F. Seidman, J.G. Seidman, Christine E. Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics |
title | Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics |
title_full | Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics |
title_fullStr | Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics |
title_full_unstemmed | Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics |
title_short | Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics |
title_sort | hypertrophic cardiomyopathy: translating cellular cross talk into therapeutics |
topic | News |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483129/ https://www.ncbi.nlm.nih.gov/pubmed/23109667 http://dx.doi.org/10.1083/jcb.201207033 |
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