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Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms
The high incidence of cardiomyopathy in patients with hemosiderosis, particularly in transfusional iron overload, strongly indicates that iron accumulation in the heart plays a major role in the process leading to heart failure. In this context, iron-mediated generation of noxious reactive oxygen sp...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4387903/ https://www.ncbi.nlm.nih.gov/pubmed/25878762 http://dx.doi.org/10.1155/2015/230182 |
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author | Gammella, Elena Recalcati, Stefania Rybinska, Ilona Buratti, Paolo Cairo, Gaetano |
author_facet | Gammella, Elena Recalcati, Stefania Rybinska, Ilona Buratti, Paolo Cairo, Gaetano |
author_sort | Gammella, Elena |
collection | PubMed |
description | The high incidence of cardiomyopathy in patients with hemosiderosis, particularly in transfusional iron overload, strongly indicates that iron accumulation in the heart plays a major role in the process leading to heart failure. In this context, iron-mediated generation of noxious reactive oxygen species is believed to be the most important pathogenetic mechanism determining cardiomyocyte damage, the initiating event of a pathologic progression involving apoptosis, fibrosis, and ultimately cardiac dysfunction. However, recent findings suggest that additional mechanisms involving subcellular organelles and inflammatory mediators are important factors in the development of this disease. Moreover, excess iron can amplify the cardiotoxic effect of other agents or events. Finally, subcellular misdistribution of iron within cardiomyocytes may represent an additional pathway leading to cardiac injury. Recent advances in imaging techniques and chelators development remarkably improved cardiac iron overload detection and treatment, respectively. However, increased understanding of the pathogenic mechanisms of iron overload cardiomyopathy is needed to pave the way for the development of improved therapeutic strategies. |
format | Online Article Text |
id | pubmed-4387903 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-43879032015-04-15 Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms Gammella, Elena Recalcati, Stefania Rybinska, Ilona Buratti, Paolo Cairo, Gaetano Oxid Med Cell Longev Review Article The high incidence of cardiomyopathy in patients with hemosiderosis, particularly in transfusional iron overload, strongly indicates that iron accumulation in the heart plays a major role in the process leading to heart failure. In this context, iron-mediated generation of noxious reactive oxygen species is believed to be the most important pathogenetic mechanism determining cardiomyocyte damage, the initiating event of a pathologic progression involving apoptosis, fibrosis, and ultimately cardiac dysfunction. However, recent findings suggest that additional mechanisms involving subcellular organelles and inflammatory mediators are important factors in the development of this disease. Moreover, excess iron can amplify the cardiotoxic effect of other agents or events. Finally, subcellular misdistribution of iron within cardiomyocytes may represent an additional pathway leading to cardiac injury. Recent advances in imaging techniques and chelators development remarkably improved cardiac iron overload detection and treatment, respectively. However, increased understanding of the pathogenic mechanisms of iron overload cardiomyopathy is needed to pave the way for the development of improved therapeutic strategies. Hindawi Publishing Corporation 2015 2015-03-24 /pmc/articles/PMC4387903/ /pubmed/25878762 http://dx.doi.org/10.1155/2015/230182 Text en Copyright © 2015 Elena Gammella et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Gammella, Elena Recalcati, Stefania Rybinska, Ilona Buratti, Paolo Cairo, Gaetano Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms |
title | Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms |
title_full | Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms |
title_fullStr | Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms |
title_full_unstemmed | Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms |
title_short | Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms |
title_sort | iron-induced damage in cardiomyopathy: oxidative-dependent and independent mechanisms |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4387903/ https://www.ncbi.nlm.nih.gov/pubmed/25878762 http://dx.doi.org/10.1155/2015/230182 |
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