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

Author:

Reilly Svetlana N.1,Liu Xing1,Carnicer Ricardo1,Recalde Alice1,Muszkiewicz Anna2,Jayaram Raja1,Carena Maria Cristina1,Wijesurendra Rohan1,Stefanini Matilde1,Surdo Nicoletta C.1,Lomas Oliver1,Ratnatunga Chandana3,Sayeed Rana3,Krasopoulos George3,Rajakumar Timothy4,Bueno-Orovio Alfonso2,Verheule Sander,Fulga Tudor A.4,Rodriguez Blanca2,Schotten Ulrich,Casadei Barbara1

Affiliation:

1. Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.

2. Department of Computer Science, University of Oxford, Oxford OX1 3QD, UK.

3. Cardiothoracic Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford OX3 9DU, UK.

4. Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK.

Abstract

Atrial microRNA-31 up-regulation causes dystrophin and nNOS depletion, which in turn contributes to the electrical phenotype of atrial fibrillation.

Funder

British Heart Foundation (BHF)

Oxford BHF Centre of Excellence

Fondation Leducq Network of Excellence

European Union 7th Framework Programme

Wellcome Trust

Weatherall Institute of Molecular Medicine

UK Medical Research Council

Wellcome Trust Senior Research Fellowship

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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