Document Detail

MicroRNAs and atrial fibrillation: mechanisms and translational potential.
MedLine Citation:
PMID:  25421165     Owner:  NLM     Status:  Publisher    
Atrial fibrillation (AF), the most common sustained arrhythmia in clinical practice, is an important contributor to cardiac morbidity and mortality. Pharmacological approaches currently available to treat patients with AF lack sufficient efficacy and are associated with potential adverse effects. Even though ablation is generally more effective than pharmacotherapy, this invasive procedure has considerable potential complications and is limited by long-term recurrences. Novel therapies based on the underlying molecular mechanisms of AF can provide useful alternatives to current treatments. MicroRNAs (miRNAs), endogenous short RNA sequences that regulate gene expression, have been implicated in the control of AF, providing novel insights into the molecular basis of the pathogenesis of AF and suggesting miRNA targeting as a potential approach for the management of this common arrhythmia. In this Review, we provide a comprehensive analysis of the current experimental evidence supporting miRNAs as important factors in AF and discuss their therapeutic implications. We first provide background information on the pathophysiology of AF and the biological determinants of miRNA synthesis and action, followed by experimental evidence for miRNA-mediated regulation of AF, and finally provide a comprehensive overview of miRNAs as potential novel therapeutic targets for AF.
Xiaobin Luo; Baofeng Yang; Stanley Nattel
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Publication Detail:
Type:  REVIEW     Date:  2014-11-25
Journal Detail:
Title:  Nature reviews. Cardiology     Volume:  -     ISSN:  1759-5010     ISO Abbreviation:  Nat Rev Cardiol     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-11-25     Completed Date:  -     Revised Date:  2014-11-26    
Medline Journal Info:
Nlm Unique ID:  101500075     Medline TA:  Nat Rev Cardiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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