Evidence map›Paper›PMID 24816040›Full record

ArticleAtherosclerosis2014

Increased atherosclerosis in mice with increased vascular biglycan content.

Joel C Thompson, Tao Tang, Patricia G Wilson, Meghan H Yoder, Lisa R Tannock

Abstract read
In one paragraph

Article in Atherosclerosis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Vascular Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Vascular smooth muscle cells in atherosclerosis.Nature reviews. Cardiology · 2019
    Review
  13. Role of serum amyloid A in atherosclerosis.Current opinion in lipidology · 2019
    Review
  14. A role for proteoglycans in vascular disease.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  15. Serum Amyloid A Is an Exchangeable Apolipoprotein.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Joel C ThompsonDivision of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
Tao TangDivision of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
Patricia G WilsonDivision of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
Meghan H YoderDivision of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA.
Lisa R TannockDivision of Endocrinology and Molecular Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, USA; Department of Veterans Affairs, Lexington, KY, USA. Electronic address: Lisa.Tannock@uky.edu.
University of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI REN, HONGMEI · 2012 to 2017
$13.7M
Angiotensin Induced Proteoglycans in AtherosclerosisR01HL082772 · NHLBI · UNIVERSITY OF KENTUCKY · PI TANNOCK, LISA R · 2007 to 2011
$2.1M
NHLBI NIH HHS R01 HL082772NHLBI NIH HHS R01HL082772NHLBI NIH HHS R01HL082772-0351NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

objectiveThe response to retention hypothesis of atherogenesis proposes that atherosclerosis is initiated via the retention of atherogenic lipoproteins by vascular proteoglycans. Co-localization studies suggest that of all the vascular proteoglycans, biglycan is the one most closely co-localized with LDL. The goal of this study was to determine if over-expression of biglycan in hyperlipidemic mice would increase atherosclerosis development.

methodsTransgenic mice were developed by expressing biglycan under control of the smooth muscle actin promoter, and were crossed to the LDL receptor deficient (C57BL/6 background) atherosclerotic mouse model. Biglycan transgenic and non-transgenic control mice were fed an atherogenic Western diet for 4-12 weeks.

resultsLDL receptor deficient mice overexpressing biglycan under control of the smooth muscle alpha actin promoter had increased atherosclerosis development that correlated with vascular biglycan content.

conclusionIncreased vascular biglycan content predisposes to increased lipid retention and increased atherosclerosis development.

Indexed as

ActinsAnimalsAtherosclerosisBiglycanBlood VesselsDisease Models, AnimalFemaleHyperlipidemiasMaleMiceMice, Inbred C57BLMice, TransgenicPromoter Regions, GeneticProteoglycansTransgenesActinsBiglycanProteoglycansAtherosclerosisBiglycanLDL retentionMice

Identifiers

PMID24816040
PMCPMC4054690
OpenAlexW2016360431

What OpenQuestion holds

Textmetadata
LicenceTDM
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.