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  • Review Article
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MicroRNAs and atrial fibrillation: mechanisms and translational potential

Nature Reviews Cardiology volume 12, pages 80–90 (2015)Cite this article

Subjects

Key Points

  • MicroRNAs are gene regulators with important pathophysiological roles in various cardiac conditions, including in atrial fibrillation (AF)

  • Patients with AF have altered microRNA expression profiles in atrial tissue and in blood

  • Correction of specific microRNA dysregulation can suppress AF in animal studies

  • Several in vivo microRNA interference approaches are under development that might be used for microRNA-targeted therapies in patients with AF in the future

  • Although microRNAs show promise as biomarkers and therapeutic targets in AF, considerable research is needed before their full potential can be realized

Abstract

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.

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Figure 1: Schematic representation of the pathophysiological mechanisms underlying AF.
Figure 2: Biogenesis and actions of miRNA.
Figure 3: miRNAs in AF-associated electrical remodelling.
Figure 4: miRNAs in AF-associated structural remodelling.
Figure 5: Strategies for miRNA-based therapies: in vivo approaches to modulate the expression or activity of miRNAs.

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Acknowledgements

The authors thank France Thériault of the Montreal Heart Institute, Montreal, QC, Canada for expert secretarial assistance, and the Canadian Institutes of Health Research and Heart and Stroke Foundation of Canada for funding.

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Authors and Affiliations

  1. Department of Medicine and Research Centre, Montreal Heart Institute and Université de Montréal, 5000 Belanger Street East, Montreal, H1T1C8, QC, Canada

    Xiaobin Luo & Stanley Nattel

  2. Department of Pharmacology, Harbin Medical University, Harbin, 150081, Heilongjiang Province, China

    Baofeng Yang

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X.L. and S.N. researched data and wrote the manuscript; all the authors contributed substantially to discussion of content, reviewing, and editing of the manuscript before submission.

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Correspondence to Stanley Nattel.

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S.N. is listed as inventor on a patent pending belonging to Montreal Heart Institute/Université de Montréal, entitled “MiR21 as a target in prevention of atrial fibrillation”. The other authors declare no competing interests.

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Luo, X., Yang, B. & Nattel, S. MicroRNAs and atrial fibrillation: mechanisms and translational potential. Nat Rev Cardiol 12, 80–90 (2015). https://doi.org/10.1038/nrcardio.2014.178

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