Evidence map›Paper›PMID 27835972›Full record

ArticleBMC cardiovascular disorders2016

The association of functional polymorphisms in genes encoding growth factors for endothelial cells and smooth muscle cells with the severity of coronary artery disease.

Tadeusz Osadnik, Joanna Katarzyna Strzelczyk, Andrzej Lekston, Rafał Reguła, Kamil Bujak, Martyna Fronczek, Marcin Gawlita, Małgorzata Gonera, Jarosław Wasilewski, Bożena Szyguła-Jurkiewicz and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2016. 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
0.9field-weighted citation impact, top 21% 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, 14 citations in OpenAlex.

  1. Article
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  4. Observational
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  8. Transforming Growth Factor-International journal of nephrology · 2018
    Article
  9. Article
  10. The Relationship betweenDisease markers · 2017
    Article
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

12 authors at 2 institutions in 1 country.

Tadeusz Osadnik2nd Department of Cardiology and Angiology, Silesian Center for Heart Diseases, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland. tadeusz.osadnik@sccs.pl.
Joanna Katarzyna StrzelczykDepartment of Medical and Molecular Biology, School of Medicine with the Division of Dentistry, Medical University of Silesia, Jordana Street 19, 41-808, Zabrze, Poland.
Andrzej Lekston3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Rafał Reguła3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Kamil Bujak3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Martyna FronczekGenomics Laboratory, Kardio-Med Silesia Science and Technology Park, Marii Curie-Skłodowskiej Street 10C, 41-800, Zabrze, Poland.
Marcin Gawlita3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Małgorzata Gonera3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Jarosław Wasilewski3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Bożena Szyguła-Jurkiewicz3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Marek Gierlotka3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Mariusz Gąsior3rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Marii Curie-Skłodowskiej Street 9, 41-800, Zabrze, Poland.
Medical University of Silesia · PLSilesian Center for Heart Disease · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite the important roles of vascular smooth muscle cells and endothelial cells in atherosclerotic lesion formation, data regarding the associations of functional polymorphisms in the genes encoding growth factors with the severity of coronary artery disease (CAD) are lacking. The aim of the present study is to analyze the relationships between functional polymorphisms in genes encoding basic fibroblast growth factor (bFGF, FGF2), epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), platelet derived growth factor-B (PDGFB), transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor A (VEGF-A) and the severity of coronary atherosclerosis in patients with stable CAD undergoing their first coronary angiography.

methodsIn total, 319 patients with stable CAD who underwent their first coronary angiography at the Silesian Centre for Heart Diseases in Zabrze, Poland were included in the analysis. CAD burden was assessed using the Gensini score. The TaqMan method was used for genotyping of selected functional polymorphisms in the FGF2, PDGFB, TGFB1, IGF1 and VEGFA genes, while rs4444903 in the EGF gene was genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The associations between the selected polymorphisms and the Gensini were calculated both for the whole cohort and for a subgroup of patients without previous myocardial infarction (MI).

resultsThere were no differences in the distribution of the Gensini score between the genotypes of the analyzed polymorphisms in FGF2, EGF, IGF1, PDFGB, and TGFB1 in the whole cohort and in the subgroup of patients without previous MI. The Gensini score for VEGFA rs699947 single-nucleotide polymorphism (SNP) in patients without previous myocardial infarction, after correction for multiple testing, was highest in patients with the A/A genotype, lower in heterozygotes and lowest in patients with the C/C genotype, (p value for trend = 0.013, false discovery rate (FDR) = 0.02). After adjustment for clinical variables, and correction for multiple comparisons the association between the VEGFA genotype and Gensini score remained only nominally significant (p = 0.04, FDR = 0.19) under the dominant genetic model in patients without previous MI.

conclusionsWe were unable to find strong association between analyzed polymorphisms in growth factors and the severity of coronary artery disease, although there was a trend toward association between rs699947 and the severity of CAD in patients without previous MI.

Indexed as

Endothelial CellsMuscle, Smooth, VascularMyocytes, Smooth MusclePolymorphism, Single NucleotideAgedCoronary AngiographyCoronary Artery DiseaseCoronary StenosisFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHeterozygoteHomozygoteHumansIntercellular Signaling Peptides and ProteinsIntercellular Signaling Peptides and ProteinsAtherosclerosisbFGFCoronary artery diseaseEGFGrowth factorsPDGFBPolymorphismTGF-β1VEGF-A

Identifiers

PMID27835972
PMCPMC5106826
OpenAlexW2556998487

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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.