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Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype?
This review focuses on cardiac atrophy resulting from mechanical or metabolic unloading due to various conditions, describing some mechanisms and discussing possible strategies or interventions to prevent, attenuate or reverse myocardial atrophy. An improved awareness of these conditions and an incr...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687767/ https://www.ncbi.nlm.nih.gov/pubmed/36359339 http://dx.doi.org/10.3390/biomedicines10112819 |
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author | Bacova, Barbara Szeiffova Andelova, Katarina Sykora, Matus Egan Benova, Tamara Barancik, Miroslav Kurahara, Lin Hai Tribulova, Narcis |
author_facet | Bacova, Barbara Szeiffova Andelova, Katarina Sykora, Matus Egan Benova, Tamara Barancik, Miroslav Kurahara, Lin Hai Tribulova, Narcis |
author_sort | Bacova, Barbara Szeiffova |
collection | PubMed |
description | This review focuses on cardiac atrophy resulting from mechanical or metabolic unloading due to various conditions, describing some mechanisms and discussing possible strategies or interventions to prevent, attenuate or reverse myocardial atrophy. An improved awareness of these conditions and an increased focus on the identification of mechanisms and therapeutic targets may facilitate the development of the effective treatment or reversion for cardiac atrophy. It appears that a decrement in the left ventricular mass itself may be the central component in cardiac deconditioning, which avoids the occurrence of life-threatening arrhythmias. The depressed myocardial contractility of atrophied myocardium along with the upregulation of electrical coupling protein, connexin43, the maintenance of its topology, and enhanced PKCε signalling may be involved in the anti-arrhythmic phenotype. Meanwhile, persistent myocardial atrophy accompanied by oxidative stress and inflammation, as well as extracellular matrix fibrosis, may lead to severe cardiac dysfunction, and heart failure. Data in the literature suggest that the prevention of heart failure via the attenuation or reversion of myocardial atrophy is possible, although this requires further research. |
format | Online Article Text |
id | pubmed-9687767 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-96877672022-11-25 Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? Bacova, Barbara Szeiffova Andelova, Katarina Sykora, Matus Egan Benova, Tamara Barancik, Miroslav Kurahara, Lin Hai Tribulova, Narcis Biomedicines Review This review focuses on cardiac atrophy resulting from mechanical or metabolic unloading due to various conditions, describing some mechanisms and discussing possible strategies or interventions to prevent, attenuate or reverse myocardial atrophy. An improved awareness of these conditions and an increased focus on the identification of mechanisms and therapeutic targets may facilitate the development of the effective treatment or reversion for cardiac atrophy. It appears that a decrement in the left ventricular mass itself may be the central component in cardiac deconditioning, which avoids the occurrence of life-threatening arrhythmias. The depressed myocardial contractility of atrophied myocardium along with the upregulation of electrical coupling protein, connexin43, the maintenance of its topology, and enhanced PKCε signalling may be involved in the anti-arrhythmic phenotype. Meanwhile, persistent myocardial atrophy accompanied by oxidative stress and inflammation, as well as extracellular matrix fibrosis, may lead to severe cardiac dysfunction, and heart failure. Data in the literature suggest that the prevention of heart failure via the attenuation or reversion of myocardial atrophy is possible, although this requires further research. MDPI 2022-11-04 /pmc/articles/PMC9687767/ /pubmed/36359339 http://dx.doi.org/10.3390/biomedicines10112819 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Bacova, Barbara Szeiffova Andelova, Katarina Sykora, Matus Egan Benova, Tamara Barancik, Miroslav Kurahara, Lin Hai Tribulova, Narcis Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? |
title | Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? |
title_full | Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? |
title_fullStr | Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? |
title_full_unstemmed | Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? |
title_short | Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype? |
title_sort | does myocardial atrophy represent anti-arrhythmic phenotype? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687767/ https://www.ncbi.nlm.nih.gov/pubmed/36359339 http://dx.doi.org/10.3390/biomedicines10112819 |
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