Document Detail

Novel insights into the cellular basis of atrial fibrillation.
MedLine Citation:
PMID:  20602552     Owner:  NLM     Status:  MEDLINE    
Atrial fibrillation is the most common clinical cardiac arrhythmia. It is often initiated by ectopic beats arising from the pulmonary veins and atria. While pulmonary vein myocytes most likely contribute to atrial ectopic beats initiating atrial fibrillation, emerging evidence suggests the existence of other cell populations that may also contribute to atrial arrhythmias. In addition to sinus node-like and intestinal Cajal-like cells, we recently characterized a novel, melanocyte-like cell population in murine and human hearts that may contribute to atrial arrhythmogenic triggers in mice. Murine cardiac melanocyte-like cells are electrically excitable, and express adrenergic and muscarinic receptors. Adult mice lacking the gene encoding dopachrome tautomerase (Dct) are susceptible to atrial arrhythmias, and Dct is expressed by both murine and human cardiac melanocytes. While Dct-expressing cells are present in human hearts in regions from which atrial arrhythmias often arise, the contribution of these cells to clinical atrial arrhythmias remains to be determined.
Vickas V Patel
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Expert review of cardiovascular therapy     Volume:  8     ISSN:  1744-8344     ISO Abbreviation:  Expert Rev Cardiovasc Ther     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-06     Completed Date:  2010-10-07     Revised Date:  2014-09-05    
Medline Journal Info:
Nlm Unique ID:  101182328     Medline TA:  Expert Rev Cardiovasc Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  907-16     Citation Subset:  IM    
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MeSH Terms
Atrial Fibrillation / etiology*,  genetics
Autonomic Nervous System / physiology
Electrophysiological Phenomena
Gene Deletion
Genetic Predisposition to Disease
Heart Atria
Intramolecular Oxidoreductases / deficiency,  genetics,  metabolism
Melanocytes / enzymology,  physiology*
Myocardium / cytology*
Myocytes, Cardiac / physiology
Pulmonary Veins / cytology
Sinoatrial Node / cytology
Thorax / blood supply
Veins / cytology
Grant Support
K08 HL074108/HL/NHLBI NIH HHS; K08 HL074108-05/HL/NHLBI NIH HHS; K08-HL074108-05/HL/NHLBI NIH HHS
Reg. No./Substance:
EC 5.3.-/Intramolecular Oxidoreductases; EC isomerase

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