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Journal article

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

Abstract:

Atrial fibrillation (AF) is a growing public health burden, and its treatment remains a challenge. AF leads to electrical remodeling of the atria, which in turn promotes AF maintenance and resistance to treatment. Although remodeling has long been a therapeutic target in AF, its causes remain poorly understood. We show that atrial-specific up-regulation of microRNA-31 (miR-31) in goat and human AF depletes neuronal nitric oxide synthase (nNOS) by accelerating mRNA decay and alters nNOS subcel...

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Publication status:
Published
Peer review status:
Peer reviewed
Version:
Accepted manuscript

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Publisher copy:
10.1126/scitranslmed.aac4296

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Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
RDM; RDM Cardiovascular Medicine
Oxford college:
Lady Margaret Hall
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
RDM; RDM Cardiovascular Medicine
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
RDM; RDM Cardiovascular Medicine
Recalde, A More by this author
More by this author
Institution:
University of Oxford
Division:
MPLS Division
Department:
Computer Science
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Publisher:
American Association for the Advancement of Science Publisher's website
Journal:
Science Translational Medicine Journal website
Volume:
8
Issue:
340
Pages:
340ra74
Publication date:
2016-05-05
Acceptance date:
2016-04-22
DOI:
EISSN:
1946-6242
ISSN:
1946-6234
Pubs id:
pubs:624186
URN:
uri:78b757aa-14ed-4a3a-b386-63764197005f
UUID:
uuid:78b757aa-14ed-4a3a-b386-63764197005f
Local pid:
pubs:624186

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