Atrial fibrillation (AF) is the most common arrhythmia worldwide and has an enormous impact on our healthcare system as it is a major contributor of morbidity and mortality. Although there are several therapeutic options available, treatment of AF still remains challenging. AF pathophysiology is complex and still incompletely understood. In general, our understanding of AF is based on two mechanistic paradigms as functional hallmarks of AF: ectopic activity and reentry. Both ectopic activity and reentry are the result of remodelling processes. Functional and/or expressional changes in ion channels, connexins or calcium-handling proteins are important factors in electrical remodelling, whereas signalling processes leading to atrial dilatation and atrial fibrosis are key factors of structural remodelling. In recent years, new intriguing key players in AF pathophysiology have been identified: microRNAs (miRNAs). MiRNAs are short, non-coding RNA fragments that can regulate gene expression and have been demonstrated as important modifiers in signalling cascades leading to electrical and structural remodelling. In this article we review the miRNA-mediated molecular mechanisms underlying AF with special emphasis on the perspective of miRNAs as potential therapeutic targets for AF treatment.
Sebastian Clauss - Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, US; University Hospital Munich, Ludwig-Maximilians University Munich; DZHK (German Centre for Cardiovascular Research), Partner Site Munich, Germany
Moritz F Sinner -University Hospital Munich, Ludwig-Maximilians University Munich
Stefan Kääb -University Hospital Munich, Ludwig-Maximilians University Munich; DZHK (German Centre for Cardiovascular Research), Partner Site Munich, Germany
Reza Wakili - University Hospital Munich, Ludwig-Maximilians University Munich; DZHK (German Centre for Cardiovascular Research), Partner Site Munich, Germany
