Evidence map›Paper›PMID 39334884›Full record

ArticleBiomolecules2024

Vascular Cytokines and Atherosclerosis: Differential Serum Levels of TRAIL, IL-18, and OPG in Obstructive Coronary Artery Disease.

Katharine A Bate, Elijah Genetzakis, Joshua Vescovi, Michael P Gray, David S Celermajer, Helen M McGuire, Stuart M Grieve, Stephen T Vernon, Siân P Cartland, Jean Y Yang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

12 authors.

Katharine A BateCardiovascular Discovery Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia.ORCID 0000-0001-9923-2722
Elijah GenetzakisCardiovascular Discovery Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia.
Joshua VescoviCardiovascular Discovery Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia.ORCID 0009-0007-0845-6204
Michael P GrayCardiovascular Discovery Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia.ORCID 0000-0003-1154-3011
David S CelermajerSchool of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW 2006, Australia.
Helen M McGuireSchool of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW 2006, Australia.ORCID 0000-0003-2047-6543
Stuart M GrieveImaging and Phenotyping Laboratory, Charles Perkins Centre, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW 2006, Australia.ORCID 0000-0002-2712-157X
Stephen T VernonCardiovascular Discovery Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia.
Siân P CartlandHeart Research Institute, The University of Sydney, Newtown, NSW 2042, Australia.ORCID 0000-0003-1723-2679
Jean Y YangSydney Precision Data Science Centre, University of Sydney, Camperdown, NSW 2006, Australia.
Mary M KavurmaHeart Research Institute, The University of Sydney, Newtown, NSW 2042, Australia.ORCID 0000-0001-7353-0932
Gemma A FigtreeCardiovascular Discovery Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia.

Funding

NHMRC Practitioner Fellowship APP11359290
6 · The paper itself

Abstract

The risk-factor-based prediction of atherosclerotic coronary artery disease (CAD) remains suboptimal, particularly in the absence of any of the standard modifiable cardiovascular risk factors (SMuRFs), making the discovery of biomarkers that correlate with atherosclerosis burden critically important. We hypothesized that cytokines and receptors associated with inflammation in CAD-tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), interleukin-18 (IL-18), and osteoprotegerin (OPG)-would be independently associated with CAD. To determine this, we measured the serum biomarker levels of 993 participants from the BioHEART study who had CT coronary angiograms that were scored for severity of stenosis and plaque composition. We found that the quartiles of TRAIL, OPG, and IL-18 were significantly associated with disease scores, and that the IL-18/TRAIL and OPG/TRAIL ratios demonstrated significant differences between no CAD vs. STEMI whereas only the OPG/TRAIL ratio showed differences between no CAD and obstructive CAD (stenosis > 50%). However, these associations did not persist after adjustment for age, sex, SMuRFs, and a family history of CAD. In conclusion, TRAIL, IL-18, and OPG and the derived ratios of IL-18/TRAIL and OPG/TRAIL demonstrate significant associations with raw disease scores and risk factors, but these markers are not discriminatory biomarkers for the prediction of CAD when incorporated into multi-variable risk models.

Indexed as

BiomarkersCoronary Artery DiseaseInterleukin-18OsteoprotegerinTNF-Related Apoptosis-Inducing LigandAgedAtherosclerosisFemaleHumansMaleMiddle AgedBiomarkersIL18 protein, humanInterleukin-18OsteoprotegerinTNF-Related Apoptosis-Inducing LigandTNFRSF11B protein, humanTNFSF10 protein, humanatherosclerosisbiomarkerscoronary artery diseasecytokinesrisk factors

Identifiers

PMID39334884
PMCPMC11430378

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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.