Evidence map›Paper›PMID 25389315›Full record

ArticleCirculation. Arrhythmia and electrophysiology2014

Loss of microRNA-106b-25 cluster promotes atrial fibrillation by enhancing ryanodine receptor type-2 expression and calcium release.

David Y Chiang, Natee Kongchan, David L Beavers, Katherina M Alsina, Niels Voigt, Joel R Neilson, Heinz Jakob, James F Martin, Dobromir Dobrev, Xander H T Wehrens and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation. Arrhythmia and electrophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 4 pooled it
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 4 syntheses or guidelines pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. 2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2018
    Guideline
  3. Pooled it
  4. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design: a report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation. Developed in partnership with the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC) and the European Cardiac Arrhythmia Society (ECAS); and in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), and the Society of Thoracic Surgeons (STS). Endorsed by the governing bodies of the American College of Cardiology Foundation, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, the Asia Pacific Heart Rhythm Society, and the Heart Rhythm Society.Heart rhythm · 2012
    Guideline
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  19. Non-coding RNA and arrhythmias: expression, function, and molecular mechanism.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
    Review
  20. Article

13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

David Y ChiangFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Natee KongchanFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
David L BeaversFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Katherina M AlsinaFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Niels VoigtFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Joel R NeilsonFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Heinz JakobFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
James F MartinFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Dobromir DobrevFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Xander H T WehrensFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.).
Na LiFrom the Cardiovascular Research Institute (D.Y.C., D.L.B., K.M.A., J.F.M., X.H.T.W., N.L.), Department of Molecular Physiology and Biophysics (D.Y.C., N.K., D.L.B., K.M.A., J.R.N., J.F.M., X.H.T.W., N.L.) Interdepartmental Program in Translational Biology and Molecular Medicine (D.Y.C., D.L.B.), Department of Medicine (Cardiology) (X.H.T.W.), Baylor College of Medicine, Houston, TX; Texas Heart Institute, Houston (J.F.M.); Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany (N.V., D.D.); and Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany (H.J.). nal@bcm.edu.
Houston Methodist · USUniversity of Duisburg-Essen · DE

Funding

Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
Research Education and Career Horizons ProgramK12GM084897 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SIFERS, RICHARD NORMAN, SLAUGHTER, GAYLE · 2008 to 2016
$8.3M
YEARS 19 - 23: BCM POST-BACCALAUREATE RESEARCH EDUCATION PROGRAMR25GM069234 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 2003 to 2024
$7.5M
Ryanodine receptor regulation in post-operative atrial fibrillationR01HL089598 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2007 to 2022
$6.5M
Pitx2 in atrial fibrillationR01HL118761 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MARTIN, JAMES F · 2014 to 2025
$6.1M
Regulation of Sarcoplasmic Reticulum Calcium Release in Heart FailureR01HL091947 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2009 to 2019
$3.2M
MicroRNAs in cleft lip and palateR01DE023177 · NIDCR · BAYLOR COLLEGE OF MEDICINE · PI MARTIN, JAMES F · 2013 to 2017
$2.8M
Determining the Role of Junctophilin-2 in Cardiac DiseaseR01HL117641 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2014 to 2017
$2.3M
Translational control of EMT by the CELF1 RNA Binding ProteinR01CA190467 · NCI · BAYLOR COLLEGE OF MEDICINE · PI NEILSON, JOEL R · 2015 to 2021
$1.9M
Development of Novel Compounds for Treatment of Heart Arrhythmias in CPVTR42HL114206 · NHLBI · ELEX BIOTECH, LLC · PI STRONGIN, ROBERT M · 2015 to 2016
$1.5M
NCI NIH HHS R01 CA190467NHLBI NIH HHS HL089598NHLBI NIH HHS HL091947NHLBI NIH HHS HL117641NHLBI NIH HHS HL118761NHLBI NIH HHS R01 HL089598NHLBI NIH HHS R01 HL091947NHLBI NIH HHS R01 HL117641NHLBI NIH HHS R01 HL118761NHLBI NIH HHS R42 HL114206NIDCR NIH HHS R01 DE023177NIGMS NIH HHS K12 GM084897NIGMS NIH HHS R25 GM056929NIGMS NIH HHS R25 GM069234
6 · The paper itself

Abstract

backgroundEnhanced sarcoplasmic reticulum Ca(2+)-leak via ryanodine receptor type-2 (RyR2) contributes to the pathogenesis of atrial fibrillation (AF). Recent studies have shown that the level of RyR2 protein is elevated in atria of patients with paroxysmal AF, suggesting that microRNA-mediated post-transcriptional regulation of RyR2 might be an underlying mechanism. Bioinformatic analysis suggests that miR-106b and miR-93, members of the miR-106b-25 cluster, could bind to RyR2-3'-untranslated region and suppress its translation. Thus, we tested the hypothesis that loss of the miR-106b-25 cluster promotes AF via enhanced RyR2-mediated sarcoplasmic reticulum Ca(2+)-leak. METHODS AND

resultsQuantitative real-time polymerase chain reaction showed that the levels of mature miR-106b, miR-93, and miR-25 were lower in atria of patients with paroxysmal AF when compared with patients in sinus rhythm. In vitro assay showed that miR-93 reduced RyR2-3'-untranslated region luciferase activity. Total RyR2 protein in atrial tissue of miR-106b-25(-/-) mice was increased by 42% when compared with wild-type littermates but still maintained a normal subcellular distribution. Ca(2+)-spark frequency and total sarcoplasmic reticulum Ca(2+)-leak were increased in atrial myocytes of miR-106b-25(-/-) mice. Telemetry ECG recordings revealed that miR-106b-25(-/-) mice exhibited more frequent atrial ectopy and were also more susceptible to pacing-induced AF than wild-type littermates. Increased sarcoplasmic reticulum Ca(2+)-release and AF susceptibility in miR-106b-25(-/-) mice were abolished by the RyR2 blocker K201.

conclusionsThese results suggest that miR-106b-25 cluster-mediated post-transcriptional regulation of RyR2 is a potential molecular mechanism involved in paroxysmal AF pathogenesis. As such, the miR-106b-25 cluster could be a novel gene-therapy target in AF associated with enhanced RyR2 expression.

Indexed as

3' Untranslated RegionsAction PotentialsAnimalsAtrial FibrillationCalciumCalcium SignalingCase-Control StudiesDisease Models, AnimalDown-RegulationGene Knockdown TechniquesHumansMice, KnockoutMicroRNAsMyocardiumRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum3' Untranslated RegionsCalciumMicroRNAsMIRN106 microRNA, humanMirn106 microRNA, mouseryanodine receptor 2. mouseRyanodine Receptor Calcium Release Channelatrial fibrillationmicroRNAryanodine receptor calcium release channel

Identifiers

PMID25389315
PMCPMC4270890
OpenAlexW2047795954

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.