Evidence map›Paper›PMID 18336235›Full record

ReviewCurrent drug targets2008

Lipoprotein size and susceptibility to atherosclerosis--insights from genetically modified mouse models.

Murielle M Véniant, Anne P Beigneux, André Bensadoun, Loren G Fong, Stephen G Young

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.6field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Article
  5. Article
  6. Animal models of human atherosclerosis: current progress.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Review
  7. Article
  8. Article
  9. T Cells in Atherosclerosis in Ldlr-/- and Apoe-/- Mice.Journal of immunological sciences · 2018
    Article
  10. Do the Apoe-/- and Ldlr-/- Mice Yield the Same Insight on Atherogenesis?Arteriosclerosis, thrombosis, and vascular biology · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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.

Murielle M VéniantAmgen Inc., One Amgen Center Drive, Thousand Oaks, CA 91320-1799, USA.
Anne P Beigneux
André Bensadoun
Loren G Fong
Stephen G Young
Amgen (United States) · US

Funding

The Lipin Protein Family and Triglyceride Metabolism P01HL090553 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2008 to 2018
$23.3M
Refining Physiologic Mechanisms for Intravascular Triglyceride MetabolismR01HL087228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEIGNEUX, ANNE, FONG, LOREN GI · 2007 to 2024
$7.8M
Hutchinson Gilford Progeria Syndrome and AtherosclerosisR01HL076839 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2005 to 2009
$1.9M
NHLBI NIH HHS P01 HL090553NHLBI NIH HHS R01 HL076839NHLBI NIH HHS R01 HL087228NHLBI NIH HHS R01 HL76839
6 · The paper itself

Abstract

High plasma levels of the apo-B-containing lipoproteins are casually implicated in the pathogenesis of atherosclerosis. This finding, backed by decades of animal and human studies, has sparked interest in defining which classes of apo-B-containing lipoprotein particles are most atherogenic. Although small LDL particles and larger remnant lipoproteins both appear to be atherogenic, it has been difficult to discern which particles are the most atherogenic. Here, we summarize several mouse models that have provided insights into this issue. The influence of lipoprotein size on susceptibility to atherosclerosis was examined by studying the phenotypes of two strains of mice with virtually identical levels of plasma cholesterol--Ldlr(-/-)Apob(100/100) and Apoe(-/-) Apob(100/100) mice. The Ldlr(-/-) Apob(100/100) mice, where the cholesterol is in small LDL particles, had far more atherosclerosis than Apoe(-/-) Apob(100/100) mice, where virtually all of the cholesterol was in larger, VLDL-sized particles. Another intriguing animal model is the Gpihbp1-deficient mouse. GPIHBP1 is an endothelial cell platform for lipolysis, and mice lacking this protein have an accumulation of large, triglyceride-rich lipoproteins. Defining the extent of atherosclerosis in these mice should provide new insights into the atherogenicity of large, triglyceride-rich lipoproteins.

Indexed as

Genetic Predisposition to DiseaseAnimalsAnimals, Genetically ModifiedAtherosclerosisDisease Models, AnimalHumansLipoproteinsMiceLipoproteins

Identifiers

PMID18336235
PMCPMC3034977
OpenAlexW2160255625

What OpenQuestion holds

Textmetadata
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.