Evidence map›Paper›PMID 22015658›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Disruption of endothelial peroxisome proliferator-activated receptor γ accelerates diet-induced atherogenesis in LDL receptor-null mice.

Aijuan Qu, Yatrik M Shah, Soumen K Manna, Frank J Gonzalez

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Novel Adipose Tissue Targets to Prevent and Treat Atherosclerosis.Handbook of experimental pharmacology · 2022
    Article
  7. Anti-inflammatory mechanisms of the vascular smooth muscle PPARγ.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. MicroRNAs in Hyperglycemia Induced Endothelial Cell Dysfunction.International journal of molecular sciences · 2016
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Pioglitazone attenuates valvular calcification induced by hypercholesterolemia.Arteriosclerosis, thrombosis, and vascular biology · 2013
    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.

Aijuan QuLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA.
Yatrik M Shah
Soumen K Manna
Frank J Gonzalez
Michigan Medicine · US

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
The role of HIF2alpha in colon carcinogenesisR01CA148828 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHAH, YATRIK M · 2010 to 2025
$5.2M
Intramural NIH HHSNCI NIH HHS CA148828NCI NIH HHS R01 CA148828
6 · The paper itself

Abstract

objectivePeroxisome proliferator-activated receptor γ (PPARγ) is widely expressed in vessel walls, and it's activation by agonists showed beneficial effects in cardiovascular diseases. However, the role of endothelial cell (EC) PPARγ in atherogenesis is not fully understood. METHODS AND

resultsTo assess the contribution of endothelial-specific PPARγ in atherosclerosis, EC-specific PPARγ disruption and LDL receptor (LDLR) double-knockout (PPARγ(ΔEC)/LDLR(-/-)) mice were developed. When challenged with a high-cholesterol diet for 4 weeks, PPARγ(ΔEC)/LDLR(-/-) mice exhibited severe atherosclerotic lesions compared to either their littermate controls or macrophage-specific PPARγ disruption and LDLR double knockout (PPARγ(ΔMΦ)/LDLR(-/-)) mice. Metabolic analysis showed severe dyslipidemia and significant increase in systolic blood pressure in the PPARγ(ΔEC)/LDLR(-/-) mice. Histological analysis and real-time quantitative PCR suggested an exacerbated inflammation in PPARγ(ΔEC)/LDLR(-/-) mice, as revealed by the increases of proinflammatory gene expression and macrophage infiltration in vivo and in vitro. Furthermore, in vivo endothelial permeability was also increased by endothelial PPARγ disruption. Bone-marrow transplantation studies, which reconstituted hematopoietic PPARγ, demonstrated that the accelerated atherogenesis was due to endothelial PPARγ deficiency.

conclusionsEndothelial PPARγ plays an important protective role in atherogenesis.

Indexed as

AnimalsAtherosclerosisBlood PressureBone Marrow TransplantationCapillary PermeabilityCholesterolDiet, AtherogenicEndothelial CellsInflammationMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutPPAR gammaReceptors, LDLCholesterolPPAR gammaReceptors, LDLTriglycerides

Identifiers

PMID22015658
PMCPMC3649072
OpenAlexW2080338463

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.