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Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress

Current therapies for arrhythmia using ion channel blockade, catheter ablation, or an implantable cardioverter defibrillator have limitations, and it is important to search for new antiarrhythmic therapeutic targets. Both atrial fibrillation and heart failure, a condition with increased arrhythmic r...

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Autor principal: Sovari, Ali A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770129/
https://www.ncbi.nlm.nih.gov/pubmed/26981310
http://dx.doi.org/10.1155/2016/9656078
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author Sovari, Ali A.
author_facet Sovari, Ali A.
author_sort Sovari, Ali A.
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description Current therapies for arrhythmia using ion channel blockade, catheter ablation, or an implantable cardioverter defibrillator have limitations, and it is important to search for new antiarrhythmic therapeutic targets. Both atrial fibrillation and heart failure, a condition with increased arrhythmic risk, are associated with excess amount of reactive oxygen species (ROS). There are several possible ways for ROS to induce arrhythmia. ROS can cause focal activity and reentry. ROS alter multiple cardiac ionic currents. ROS promote cardiac fibrosis and impair gap junction function, resulting in reduced myocyte coupling and facilitation of reentry. In order to design effective antioxidant drugs for treatment of arrhythmia, it is essential to explore the molecular mechanisms by which ROS exert these arrhythmic effects. Activation of Ca(2+)/CaM-dependent kinase II, c-Src tyrosine kinase, protein kinase C, and abnormal splicing of cardiac sodium channels are among the recently discovered molecular mechanisms of ROS-induced arrhythmia.
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spelling pubmed-47701292016-03-15 Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress Sovari, Ali A. Cardiol Res Pract Review Article Current therapies for arrhythmia using ion channel blockade, catheter ablation, or an implantable cardioverter defibrillator have limitations, and it is important to search for new antiarrhythmic therapeutic targets. Both atrial fibrillation and heart failure, a condition with increased arrhythmic risk, are associated with excess amount of reactive oxygen species (ROS). There are several possible ways for ROS to induce arrhythmia. ROS can cause focal activity and reentry. ROS alter multiple cardiac ionic currents. ROS promote cardiac fibrosis and impair gap junction function, resulting in reduced myocyte coupling and facilitation of reentry. In order to design effective antioxidant drugs for treatment of arrhythmia, it is essential to explore the molecular mechanisms by which ROS exert these arrhythmic effects. Activation of Ca(2+)/CaM-dependent kinase II, c-Src tyrosine kinase, protein kinase C, and abnormal splicing of cardiac sodium channels are among the recently discovered molecular mechanisms of ROS-induced arrhythmia. Hindawi Publishing Corporation 2016 2016-02-15 /pmc/articles/PMC4770129/ /pubmed/26981310 http://dx.doi.org/10.1155/2016/9656078 Text en Copyright © 2016 Ali A. Sovari. https://creativecommons.org/licenses/by/4.0/ 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
Sovari, Ali A.
Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress
title Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress
title_full Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress
title_fullStr Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress
title_full_unstemmed Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress
title_short Cellular and Molecular Mechanisms of Arrhythmia by Oxidative Stress
title_sort cellular and molecular mechanisms of arrhythmia by oxidative stress
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770129/
https://www.ncbi.nlm.nih.gov/pubmed/26981310
http://dx.doi.org/10.1155/2016/9656078
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