Evidence map›Paper›PMID 19910639›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

Genetic association and interaction analysis of USF1 and APOA5 on lipid levels and atherosclerosis.

Pirkka-Pekka Laurila, Jussi Naukkarinen, Kati Kristiansson, Samuli Ripatti, Tuuli Kauttu, Kaisa Silander, Veikko Salomaa, Markus Perola, Pekka J Karhunen, Philip J Barter and 2 more

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Effects ofFrontiers in cardiovascular medicine · 2022
    Article
  6. Article
  7. Review
  8. Review
  9. Network motif-based method for identifying coronary artery disease.Experimental and therapeutic medicine · 2016
    Article
  10. Article
  11. Significant association between upstream transcription factor 1 rs2516839 polymorphism and hepatocellular carcinoma risk: a case-control study.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. The genetics of familial combined hyperlipidaemia.Nature reviews. Endocrinology · 2012
    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 at 5 institutions in 2 countries.

Pirkka-Pekka LaurilaPublic Health Genomics Unit, National Institute for Health and Welfare and Institute for Molecular Medicine, Helsinki, Finland.
Jussi Naukkarinen
Kati Kristiansson
Samuli Ripatti
Tuuli Kauttu
Kaisa Silander
Veikko Salomaa
Markus Perola
Pekka J Karhunen
Philip J Barter
Christian Ehnholm
Leena Peltonen
University of Helsinki · FIWellcome Sanger Institute · GBTampere University · FIFinnish Institute for Health and Welfare · FITampere University · FI

Funding

Wellcome Trust 089061
6 · The paper itself

Abstract

objectiveUSF1 is a ubiquitous transcription factor governing the expression of numerous genes of lipid and glucose metabolism. APOA5 is a well-established candidate gene regulating triglyceride (TG) levels and has been identified as a downstream target of upstream stimulatory factor. No detailed studies about the effect of APOA5 on atherosclerotic lesion formation have been conducted, nor has its potential interaction with USF1 been examined. METHODS AND

resultsWe analyzed allelic variants of USF1 and APOA5 in families (n=516) ascertained for atherogenic dyslipidemia and in an autopsy series of middle-aged men (n=300) with precise quantitative measurements of atherosclerotic lesions. The impact of previously associated APOA5 variants on TGs was observed in the dyslipidemic families, and variant rs3135506 was associated with size of fibrotic aortic lesions in the autopsy series. The USF1 variant rs2516839, associated previously with atherosclerotic lesions, showed an effect on TGs in members of the dyslipidemic families with documented coronary artery disease. We provide preliminary evidence of gene-gene interaction between these variants in an autopsy series with a fibrotic lesion area in the abdominal aorta (P=0.0028), with TGs in dyslipidemic coronary artery disease subjects (P=0.03), and with high-density lipoprotein cholesterol (P=0.008) in a large population cohort of coronary artery disease patients (n=1065) in which the interaction for TGs was not replicated.

conclusionsOur findings in these unique samples reinforce the roles of APOA5 and USF1 variants on cardiovascular phenotypes and suggest that both genes contribute to lipid levels and aortic atherosclerosis individually and possibly through epistatic effects.

Indexed as

Epistasis, GeneticAdultAorta, AbdominalAortic DiseasesApolipoprotein A-VApolipoproteins AAtherosclerosisAustraliaAutopsyCholesterol, HDLCholesterol, LDLCoronary Artery DiseaseDyslipidemiasFemaleFibrosisFinlandAPOA5 protein, humanApolipoprotein A-VApolipoproteins ACholesterol, HDLCholesterol, LDLLipidsTriglyceridesUpstream Stimulatory FactorsUSF1 protein, human

Identifiers

PMID19910639
PMCPMC3224996
OpenAlexW2097417967

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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.