Evidence map›Paper›PMID 28686695›Full record

ArticlePloS one2017

Coronary artery disease-associated genetic variants and biomarkers of inflammation.

Morten Krogh Christiansen, Sanne Bøjet Larsen, Mette Nyegaard, Søs Neergaard-Petersen, Ramzi Ajjan, Morten Würtz, Erik Lerkevang Grove, Anne-Mette Hvas, Henrik Kjærulf Jensen, Steen Dalby Kristensen

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Improving T2D machine learning-based prediction accuracy with SNPs and younger age.Computational and structural biotechnology journal · 2025
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  11. Association of functionalOncotarget · 2020
    Article
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  13. Article
  14. Genetic and epigenetic regulation of human aging and longevity.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  15. Review
  16. Article
  17. 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

10 authors.

Morten Krogh ChristiansenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.ORCID http://orcid.org/0000-0002-3894-888X
Sanne Bøjet LarsenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Mette NyegaardDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Søs Neergaard-PetersenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Ramzi AjjanLeeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, United Kingdom.
Morten WürtzDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Erik Lerkevang GroveDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Anne-Mette HvasFaculty of Health, Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Henrik Kjærulf JensenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Steen Dalby KristensenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGenetic constitution and inflammation both contribute to development of coronary artery disease (CAD). Several CAD-associated single-nucleotide polymorphisms (SNPs) have recently been identified, but their functions are largely unknown. We investigated the associations between CAD-associated SNPs and five CAD-related inflammatory biomarkers.

methodsWe genotyped 45 CAD-associated SNPs in 701 stable CAD patients in whom levels of high-sensitivity C-reactive protein (hsRCP), interleukin-6, calprotectin, fibrinogen and complement component 3 levels had previously been measured. A genetic risk score was calculated to assess the combined risk associated with all the genetic variants. A multiple linear regression model was used to assess associations between the genetic risk score, single SNPs, and the five inflammatory biomarkers.

resultsThe minor allele (G) (CAD risk allele) of rs2075650 (TOMM40/APOE) was associated with lower levels of high-sensitivity C-reactive protein (effect per risk allele: -0.37 mg/l [95%CI -0.56 to -0.18 mg/l]). The inflammatory markers tested showed no association with the remaining 44 SNPs or with the genetic risk score.

conclusionsIn stable CAD patients, the risk allele of a common CAD-associated marker at the TOMM40/APOE locus was associated with lower hsCRP levels. No other genetic variants or the combined effect of all variants were associated with the five inflammatory biomarkers.

Indexed as

AllelesGenetic LociPolymorphism, Single NucleotideAdultAgedAged, 80 and overApolipoproteins EBiomarkersComplement C3Coronary Artery DiseaseC-Reactive ProteinCross-Sectional StudiesFemaleFibrinogenGene ExpressionHumansApolipoproteins EBiomarkersC3 protein, humanComplement C3C-Reactive ProteinFibrinogenIL6 protein, humanInterleukin-6Leukocyte L1 Antigen ComplexMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsTOMM40 protein, human

Identifiers

PMID28686695
PMCPMC5501546

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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.