Evidence map›Paper›PMID 26088132›Full record

ArticleThe Journal of biological chemistry2015

Absence of the Regulator of G-protein Signaling, RGS4, Predisposes to Atrial Fibrillation and Is Associated with Abnormal Calcium Handling.

Aaisha Opel, Muriel Nobles, David Montaigne, Malcolm Finlay, Naomi Anderson, Ross Breckenridge, Andrew Tinker

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. iScience · 2024
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  16. The therapeutic potential of targeting cardiac RGS4.Therapeutic advances in cardiovascular disease
    Review
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

7 authors at 2 institutions in 1 country.

Aaisha OpelFrom the British Heart Foundation Laboratories, Department of Medicine, University College London, Rayne Institute, London WC1E 6JJ, United Kingdom and the William Harvey Heart Centre, Barts & The London School of Medicine & Dentistry, London EC1M 6BQ, United Kingdom.
Muriel Noblesthe William Harvey Heart Centre, Barts & The London School of Medicine & Dentistry, London EC1M 6BQ, United Kingdom.
David Montaignethe William Harvey Heart Centre, Barts & The London School of Medicine & Dentistry, London EC1M 6BQ, United Kingdom.
Malcolm Finlaythe William Harvey Heart Centre, Barts & The London School of Medicine & Dentistry, London EC1M 6BQ, United Kingdom.
Naomi Andersonthe William Harvey Heart Centre, Barts & The London School of Medicine & Dentistry, London EC1M 6BQ, United Kingdom.
Ross BreckenridgeFrom the British Heart Foundation Laboratories, Department of Medicine, University College London, Rayne Institute, London WC1E 6JJ, United Kingdom and.
Andrew TinkerFrom the British Heart Foundation Laboratories, Department of Medicine, University College London, Rayne Institute, London WC1E 6JJ, United Kingdom and the William Harvey Heart Centre, Barts & The London School of Medicine & Dentistry, London EC1M 6BQ, United Kingdom a.tinker@qmul.ac.uk.
Queen Mary University of London · GBUniversity College London · GB

Funding

British Heart Foundation FS/09/042/27860Wellcome TrustWellcome Trust 081475/Z/06/Z
6 · The paper itself

Abstract

The description of potential molecular substrates for predisposition to atrial fibrillation (AF) is incomplete, and it is unknown what role regulators of G-protein signaling might play. We address whether the attenuation of RGS4 function may promote AF and the mechanism through which this occurs. For this purpose, we studied a mouse with global genetic deletion of RGS4 (RGS4(-/-)) and the normal littermate controls (RGS4(+/+)). In vivo electrophysiology using atrial burst pacing revealed that mice with global RGS4 deletion developed AF more frequently than control littermates. Isolated atrial cells from RGS4(-/-) mice show an increase in Ca(2+) spark frequency under basal conditions and after the addition of endothelin-1 and abnormal spontaneous Ca(2+) release events after field stimulation. Isolated left atria studied on a multielectrode array revealed modest changes in path length for re-entry but abnormal electrical events after a pacing train in RGS4(-/-) mice. RGS4 deletion results in a predisposition to atrial fibrillation from enhanced activity in the Gαq/11-IP3 pathway, resulting in abnormal Ca(2+) release and corresponding electrical events.

Indexed as

Action PotentialsAnimalsAtrial FibrillationCalciumCalcium SignalingElectric StimulationGenetic Predisposition to DiseaseHeart AtriaMice, Inbred C57BLMice, KnockoutMyocytes, CardiacRGS ProteinsCalciumRGS4 proteinRGS Proteinsarrhythmiaatrial fibrillationcalciumcardiac musclecell signalingelectrophysiologyinositol 1,4,5-trisphosphate (IP3)regulator of G protein signaling (RGS)

Identifiers

PMID26088132
PMCPMC4521044
OpenAlexW1470476341

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.