Evidence map›Paper›PMID 23950981›Full record

ArticlePloS one2013

Pathway analysis using genome-wide association study data for coronary restenosis--a potential role for the PARVB gene.

Jeffrey J W Verschuren, Stella Trompet, M Lourdes Sampietro, Bastiaan T Heijmans, Werner Koch, Adnan Kastrati, Jeanine J Houwing-Duistermaat, P Eline Slagboom, Paul H A Quax, J Wouter Jukema

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Jeffrey J W VerschurenDepartment of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Stella Trompet
M Lourdes Sampietro
Bastiaan T Heijmans
Werner Koch
Adnan Kastrati
Jeanine J Houwing-Duistermaat
P Eline Slagboom
Paul H A Quax
J Wouter Jukema
Leiden University Medical Center · NLDeutsches Herzzentrum München · DENetherlands Consortium for Healthy Ageing · NLNetherlands Heart Institute · NLTechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary restenosis after percutaneous coronary intervention (PCI) still remains a significant limitation of the procedure. The causative mechanisms of restenosis have not yet been fully identified. The goal of the current study was to perform gene-set analysis of biological pathways related to inflammation, proliferation, vascular function and transcriptional regulation on coronary restenosis to identify novel genes and pathways related to this condition.

methodsThe GENetic DEterminants of Restenosis (GENDER) databank contains genotypic data of 556,099SNPs of 295 cases with restenosis and 571 matched controls. Fifty-four pathways, related to known restenosis-related processes, were selected. Gene-set analysis was performed using PLINK, GRASS and ALIGATOR software. Pathways with a p<0.01 were fine-mapped and significantly associated SNPs were analyzed in an independent replication cohort.

resultsSix pathways (cell-extracellular matrix (ECM) interactions pathway, IL2 signaling pathway, IL6 signaling pathway, platelet derived growth factor pathway, vitamin D receptor pathway and the mitochondria pathway) were significantly associated in one or two of the software packages. Two SNPs in the cell-ECM interactions pathway were replicated in an independent restenosis cohort. No replication was obtained for the other pathways.

conclusionWith these results we demonstrate a potential role of the cell-ECM interactions pathway in the development of coronary restenosis. These findings contribute to the increasing knowledge of the genetic etiology of restenosis formation and could serve as a hypothesis-generating effort for further functional studies.

Indexed as

Genetic Predisposition to DiseaseActininAgedCase-Control StudiesCoronary RestenosisCytokinesEndothelial CellsEndothelium, VascularExtracellular MatrixFemaleGene Expression RegulationGenome-Wide Association StudyHumansMaleMetabolic Networks and PathwaysMiddle AgedActininCytokinesPARVB protein, human

Identifiers

PMID23950981
PMCPMC3739784
OpenAlexW1975851234

What Socratic holds

Textmetadata
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 Socratic graph.