Evidence map›Paper›PMID 26252659›Full record

ArticlePloS one2015

Identification of Region-Specific Myocardial Gene Expression Patterns in a Chronic Swine Model of Repaired Tetralogy of Fallot.

Sabine Charron, François Roubertie, David Benoist, Virginie Dubes, Stephen H Gilbert, Marion Constantin, Delphine Vieillot, Delphine Elbes, Bruno Quesson, Pierre Bordachar and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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  10. Large Mammalian Animal Models of Heart Disease.Journal of cardiovascular development and disease · 2016
    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

14 authors at 1 institution in 3 countries.

Sabine CharronL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France.
François RoubertieL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France; Hôpital cardiologique Haut-Lévêque, CHU de Bordeaux, Pessac, France.
David BenoistL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France.
Virginie DubesL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France.
Stephen H GilbertL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France; Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Marion ConstantinL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France.
Delphine VieillotPlateforme Technologique d'Innovation Biomédicale, Université de Bordeaux, Pessac, France.
Delphine ElbesL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France; University of Oxford, Institute of Biomedical Engineering, Oxford, United-Kingdom.
Bruno QuessonL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France.
Pierre BordacharL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France; Hôpital cardiologique Haut-Lévêque, CHU de Bordeaux, Pessac, France.
Michel HaissaguerreL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France; Hôpital cardiologique Haut-Lévêque, CHU de Bordeaux, Pessac, France.
Olivier BernusL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France.
Jean-Benoit ThamboL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Inserm U1045 CRCTB, Université de Bordeaux, Bordeaux, France; Hôpital cardiologique Haut-Lévêque, CHU de Bordeaux, Pessac, France.
Caroline RooryckL'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Université de Bordeaux, Pessac, France; Hôpital cardiologique Haut-Lévêque, CHU de Bordeaux, Pessac, France; Laboratoire Maladies Rares: Génétique et Métabolisme (MRGM), EA 4576, Université de Bordeaux, Bordeaux, France.
Université de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Surgical repair of Tetralogy of Fallot (TOF) is highly successful but may be complicated in adulthood by arrhythmias, sudden death, and right ventricular or biventricular dysfunction. To better understand the molecular and cellular mechanisms of these delayed cardiac events, a chronic animal model of postoperative TOF was studied using microarrays to perform cardiac transcriptomic studies. The experimental study included 12 piglets (7 rTOF and 5 controls) that underwent surgery at age 2 months and were further studied after 23 (+/- 1) weeks of postoperative recovery. Two distinct regions (endocardium and epicardium) from both ventricles were analyzed. Expression levels from each localization were compared in order to decipher mechanisms and signaling pathways leading to ventricular dysfunction and arrhythmias in surgically repaired TOF. Several genes were confirmed to participate in ventricular remodeling and cardiac failure and some new candidate genes were described. In particular, these data pointed out FRZB as a heart failure marker. Moreover, calcium handling and contractile function genes (SLN, ACTC1, PLCD4, PLCZ), potential arrhythmia-related genes (MYO5B, KCNA5), and cytoskeleton and cellular organization-related genes (XIRP2, COL8A1, KCNA6) were among the most deregulated genes in rTOF ventricles. To our knowledge, this is the first comprehensive report on global gene expression profiling in the heart of a long-term swine model of repaired TOF.

Indexed as

Gene Expression RegulationAnimalsChronic DiseaseDisease Models, AnimalEndocardiumGene Expression ProfilingGene OntologyGene Regulatory NetworksGenetic Association StudiesHeart VentriclesMyocardiumOligonucleotide Array Sequence AnalysisOrgan SpecificityReal-Time Polymerase Chain ReactionReproducibility of ResultsSus scrofa

Identifiers

PMID26252659
PMCPMC4529093
OpenAlexW1767427105

What OpenQuestion holds

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LicenceCC BY
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.