Evidence map›Paper›PMID 22228203›Full record

ArticlePharmacogenetics and genomics2012

A genome-wide association study of inflammatory biomarker changes in response to fenofibrate treatment in the Genetics of Lipid Lowering Drug and Diet Network.

Stella Aslibekyan, Edmond K Kabagambe, Marguerite R Irvin, Robert J Straka, Ingrid B Borecki, Hemant K Tiwari, Michael Y Tsai, Paul N Hopkins, Jian Shen, Chao-Qiang Lai and 2 more

Abstract read
In one paragraph

Article in Pharmacogenetics and genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 4 pooled it
5.8field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 4 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Review
  9. Role of fenofibrate in multiple sclerosis.European journal of medical research · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Article
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  19. Article
  20. Oncotarget · 2018
    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 6 institutions in 2 countries.

Stella AslibekyanDepartments of Epidemiology, School of Public Health, University of Alabama at Birmingham, Alabama, USA. saslibek@uab.edu
Edmond K Kabagambe
Marguerite R Irvin
Robert J Straka
Ingrid B Borecki
Hemant K Tiwari
Michael Y Tsai
Paul N Hopkins
Jian Shen
Chao-Qiang Lai
Jose M Ordovas
Donna K Arnett
Madrid Institute for Advanced Studies · ESAlabama Department of Public Health · USUniversity of Alabama at Birmingham · USUniversity of Minnesota · USUniversity of Utah · USWashington University in St. Louis · US

Funding

Genetic and Environmental Determinants of TriglyceridesU01HL072524 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K · 2002 to 2008
$11.9M
NHLBI NIH HHS U01 HL072524NHLBI NIH HHS U01HL072524-04
6 · The paper itself

Abstract

objectiveDespite the evidence in support of the anti-inflammatory and triglyceride-lowering effects of fenofibrate, little is known about genetic determinants of the observed heterogeneity in treatment response. This study provides the first genome-wide examination of fenofibrate effects on systemic inflammation.

methodsBiomarkers of inflammation were measured in participants of the Genetics of Lipid Lowering Drugs and Diet Network (n=1092) before and after a 3-week daily treatment with 160 mg of fenofibrate. Two inflammatory patterns [high-sensitivity C-reactive protein-interleukin-6 and monocyte chemoattractant protein-1-tumor necrosis factor (MCP1-TNF-α)] were derived using principal component analysis. Associations between single nucleotide polymorphisms on the Affymetrix 6.0 chip and phenotypes were assessed using mixed linear models, adjusted for age, sex, study center, and ancestry as fixed effects and pedigree as a random effect.

resultsBefore fenofibrate treatment, the strongest evidence for association was observed for polymorphisms near or within the IL2RA gene with the high-sensitivity C-reactive protein-interleukin-6 (IL6) pattern (rs7911500, P=5×10 and rs12722605, P=5×10). Associations of the MCP1-TNF-α pattern with loci in several biologically plausible genes [CYP4F8 (rs3764563), APBB1IP (rs1775246), COL13A1 (rs2683572), and COMMD10 (rs1396485)] approached genome-wide significance (P=3×10, 5×10, 6×10, and 7×10, respectively) before fenofibrate treatment. After fenofibrate treatment, the rs12722605 locus in IL2RA was also associated with the MCP1-TNF-α pattern (P=3×10). The analyses of individual biomarker response to fenofibrate did not yield genome-wide significant results, but the rs6517147 locus near the immunologically relevant IFNAR2 gene was suggestively associated with IL6 (P=7×10).

conclusionWe have identified several novel biologically relevant loci associated with systemic inflammation before and after fenofibrate treatment.

Indexed as

Genome-Wide Association StudyAdultChemokine CCL2C-Reactive ProteinFemaleFenofibrateGene FrequencyGenotyping TechniquesHumansHypolipidemic AgentsInflammationInterleukin-2 Receptor alpha SubunitInterleukin-6MaleMiddle AgedPolymorphism, Single NucleotideCCL2 protein, humanChemokine CCL2C-Reactive ProteinFenofibrateHypolipidemic AgentsIL2RA protein, humanInterleukin-2 Receptor alpha SubunitInterleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID22228203
PMCPMC3275691
OpenAlexW2076973731

What OpenQuestion holds

Textmetadata
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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.