Research ArticleCardiovascular Disease

Up-regulation of miR-31 in human atrial fibrillation begets the arrhythmia by depleting dystrophin and neuronal nitric oxide synthase

See allHide authors and affiliations

Science Translational Medicine  25 May 2016:
Vol. 8, Issue 340, pp. 340ra74
DOI: 10.1126/scitranslmed.aac4296

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Rhythm remodeling traced to tiny RNA

Atrial fibrillation (AF) is characterized by abnormal heart rhythms and can be caused by a variety of risk factors ranging from obesity to diabetes. Although treatments exist, AF is famously able to recur by “remodeling” the heart tissue electrically and structurally to maintain its unsteady beat. Reilly et al. have discovered a small noncoding RNA, miR-31, that is responsible for a string of signals that allow for such remodeling. An increase in miR-31 led to depletion of neuronal nitric oxide synthase (nNOS) and repression of dystrophin (which binds nNOS in muscle cells) in the fibrillating atrial myocardium of both humans and goats. These mechanistic findings were further explored in mice. Because up-regulation of miR-31 and the resulting loss of dystrophin and nNOS in AF are specific to the atrium, it may be possible to target interventions to this remodeling pathway, thus providing a safer therapeutic option for patients with AF than those that are currently available, including ablation and ion channel blockers.

View Full Text

Stay Connected to
   Science Translational Medicine