Evidence map›Paper›PMID 20133902›Full record

ArticleCirculation research2010

Aortic arch curvature and atherosclerosis have overlapping quantitative trait loci in a cross between 129S6/SvEvTac and C57BL/6J apolipoprotein E-null mice.

Hirofumi Tomita, Svetlana Zhilicheva, Shinja Kim, Nobuyo Maeda

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  3. Role of shear stress-induced red blood cell released ATP in atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2025
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  5. Insights from Murine Studies on the Site Specificity of Atherosclerosis.International journal of molecular sciences · 2024
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  7. Life (Basel, Switzerland) · 2022
    Article
  8. Reduction ofFrontiers in cardiovascular medicine · 2022
    Article
  9. Pig and Mouse Models of Hyperlipidemia and Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Genetic analysis of a mouse cross implicates an anti-inflammatory gene in control of atherosclerosis susceptibility.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
    Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Hirofumi TomitaDepartment of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7525, USA.
Svetlana Zhilicheva
Shinja Kim
Nobuyo Maeda
University of North Carolina at Chapel Hill · US

Funding

APOLIPOROTEIN GENES AND ATHEROGENESISR01HL042630 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1989 to 2017
$4.9M
APOLIPOPROTEIN GENES AND ATHEROGENESIS IN ANIMALSR37HL042630 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1998 to 2007
$3.4M
NHLBI NIH HHS HL42630NHLBI NIH HHS R01 HL042630NHLBI NIH HHS R37 HL042630
6 · The paper itself

Abstract

rationaleApolipoprotein E-null mice with a 129S6/SvEvTac strain background (129-apoE) develop atherosclerotic plaques faster in the aortic arch but slower in the aortic root than those with a C57BL/6J background (B6-apoE). The shape of the aortic arch also differs in the 2 strains.

objectiveBecause circulating plasma factors are the same at both locations, we tested the hypothesis that genetic factors affecting vascular geometry also affect the location and extent of atherosclerotic plaque development. METHODS AND

resultsTests on the F2 progeny from a cross between 129-apoE-null and B6-apoE-null mice showed that the extent of atherosclerosis in the aortic arch is significantly correlated in males, but not in females, with the shape of arch curvature (r=0.34, P<0.0001) and weakly with the arch diameter (r=0.20, P=0.02). Quantitative trait locus (QTL) analysis identified 2 significant peaks for aortic arch lesion size on chromosome 1 (105 Mb, LOD=5.0, and 163 Mb, LOD=6.8), and a suggestive QTL on chromosome 15 (96 Mb, LOD=4.7). A significant QTL for aortic root lesion size was on chromosome 9 (61 Mb, LOD=6.9), but it was distinct from the QTLs for arch lesion size. Remarkably, the QTLs for susceptibility to atherosclerosis in the arch overlapped with a significant QTL that affects curvature of the arch on chromosome 1 (121 Mb, LOD=5.6) and a suggestive QTL on chromosome 15 (76 Mb, LOD=3.5).

conclusionsThe overlapping QTLs for curvature of the aortic arch and atherosclerosis support that the ontogeny of the aortic arch formation is a potential risk factor for atherosclerosis.

Indexed as

Chromosomes, MammalianQuantitative Trait LociAnimalsAorta, ThoracicApolipoproteins EAtherosclerosisCrosses, GeneticDisease Models, AnimalFemaleGene Expression Regulation, DevelopmentalGenetic Predisposition to DiseaseHeredityLipidsMaleMiceMice, Inbred C57BLApolipoproteins ELipids

Identifiers

PMID20133902
PMCPMC2848914
OpenAlexW2122823608

What OpenQuestion holds

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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.