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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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Institution:
University of Oxford
Department:
Oxford, MSD, RDM, RDM Cardiovascular Medicine
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Institution:
University of Oxford
Department:
Oxford, MSD, RDM, RDM Cardiovascular Medicine
More by this author
Institution:
University of Oxford
Department:
Oxford, MSD, RDM, RDM Cardiovascular Medicine
More by this author
Institution:
University of Oxford
Department:
Oxford, MSD, RDM, RDM Cardiovascular Medicine
More by this author
Institution:
University of Oxford
Department:
Oxford, MPLS, Computer Science
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Grant:
RG/11/15/29375; RE/13/1/3018
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Grant:
(FP7/2007-2013) n°261057 EUTRAF; Marie Curie RADOX Grant
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Grant:
099898/Z/12/Z; 100246/Z/12/Z
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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:
340ra74-340ra74
Publication date:
2016-05-25
DOI:
EISSN:
1946-6242
ISSN:
1946-6234
URN:
uuid:da22a05e-ac7d-401a-8a32-87ab8a71c90d
Source identifiers:
624186
Local pid:
pubs:624186

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