| Pathological remodeling of cardiac gap junction connexin 43-With special reference to arrhythmogenesis. | |
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MedLine Citation:
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PMID: 19540736 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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A dysfunction of the cardiac gap junction, which contributes to electrical cell-to-cell coupling is one of essential factors known to generate arrhythmias. The function of the gap junction depends on the regulation of connexin which composes the gap junction channel. A dysfunction of the gap junction is possibly caused by the down-regulation of connexin. In this review, the relationship between pathological remodeling of connexin 43 (Cx43) and susceptibility of the heart to the ventricular fibrillation, which is a lethal ventricular tachyarrhythmia, is addressed. A suppression of the PKA-mediated phosphorylation or an augmentation of the PKC-mediated phosphorylation of Cx43 induces the downward remodeling of Cx43. Factors regarding downward remodeling of Cx43, such as hypoxia (including intracellular Ca overload and intracellular acidosis), angiotensin II or an activation of PKCvarepsilon make the heart more susceptible to the ventricular fibrillation, while factors regarding upward remodeling of Cx43, such as cyclic AMP or an activation of PKA, lower susceptibility. As a result, from a clinical point of view, angiotensin II antagonists (synthesis inhibitors or receptor blockades), PKC inhibitors or PKA activators are thus considered to provide a therapeutic approach for the treatment of the initiation or advancement of the ventricular fibrillation. |
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Authors:
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Issei Imanaga |
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Publication Detail:
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Type: Journal Article Date: 2009-06-21 |
Journal Detail:
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Title: Pathophysiology : the official journal of the International Society for Pathophysiology / ISP Volume: 17 ISSN: 0928-4680 ISO Abbreviation: Pathophysiology Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-09 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9433813 Medline TA: Pathophysiology Country: Netherlands |
Other Details:
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Languages: eng Pagination: 73-81 Citation Subset: - |
Copyright Information:
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Copyright © 2009 Elsevier Ireland Ltd. All rights reserved. |
Affiliation:
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Department of Physiology, Fukuoka University, Faculty of Medicine, Health Care Center, Nagomi Sato, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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