| Molecular mechanisms of remodeling in human atrial fibrillation. | |
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MedLine Citation:
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PMID: 12062337 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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An important acknowledgement of the last several years is that atrial fibrillation (AF) modifies the electrical properties of the atrium in a way that promotes its occurrence and maintenance. This arrhythmogenic electrophysiological remodeling is well established, but can not explain by itself that 'AF begets AF'. This review describes molecular changes involving rapid functional alterations and slower changes in protein expression that cause electrical remodeling and contractile dysfunction in AF. An important molecular feature of AF is the reduction in L-type Ca(2+) channel function and protein expression. This reduction may serve to protect the cell against a potentially lethal Ca(2+) overload resulting from the increased activation rate in AF. Further, the review discusses the possible role of proteolytic systems, notably the calpains, as a mechanism linking Ca(2+) overload to reduced protein expression. Thus, it appears that the elaborate molecular changes in AF are directed primarily at protecting the myocyte from cellular stress. However, such early protection occurs at the expense of electrophysiological changes that promote the long-term maintenance of AF. |
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Authors:
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Bianca J J M Brundel; Robert H Henning; Harm H Kampinga; Isabelle C Van Gelder; Harry J G M Crijns |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Cardiovascular research Volume: 54 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2002 May |
Date Detail:
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Created Date: 2002-06-13 Completed Date: 2002-07-12 Revised Date: 2005-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 315-24 Citation Subset: IM |
Affiliation:
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Department of Radiation and Stress Cell Biology, University of Groningen, A. Deusinglaan 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands. B.J.J.M.Brundel@med.rug.nl |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Atrial Fibrillation / etiology*, metabolism, physiopathology Atrial Function* Calcium / metabolism Calcium Channels, L-Type / genetics*, metabolism Calpain / metabolism Cardiac Pacing, Artificial Chronic Disease Connexins / metabolism Gene Expression Heart Atria / pathology Humans |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channels, L-Type; 0/Connexins; 7440-70-2/Calcium; EC 3.4.22.-/Calpain |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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