Evidence map›Paper›PMID 17110163›Full record

ArticleBiochimica et biophysica acta2006

Effects of FXR in foam-cell formation and atherosclerosis development.

Grace L Guo, Silvia Santamarina-Fojo, Taro E Akiyama, Marcelo J A Amar, Beverly J Paigen, Bryan Brewer, Frank J Gonzalez

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

65 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. FXR Friend-ChIPs in the Enterohepatic System.Seminars in liver disease · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Diet-gut microbiota interactions on cardiovascular disease.Computational and structural biotechnology journal · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Regulation of Lung Macrophage Activation and Oxidative Stress Following Ozone Exposure by Farnesoid X Receptor.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Grace L GuoLaboratory of Metabolism, Bldg. 37, Rm. 3106B, NCI, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA.
Silvia Santamarina-Fojo
Taro E Akiyama
Marcelo J A Amar
Beverly J Paigen
Bryan Brewer
Frank J Gonzalez
National Institutes of Health · USJackson Laboratory · US

Funding

Xenobiotic ReceptorsZ01BC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 1996 to 2008
$1.7M
Intramural NIH HHSNCI NIH HHS Z01 BC005708-14
6 · The paper itself

Abstract

Farnesoid X receptor (FXR), a bile-acid-activated member of the nuclear receptor superfamily, is essential in regulating bile-acid, cholesterol, and triglyceride homeostasis. Disruption of the FXR gene in mice results in a proatherosclerotic lipid profile with increased serum cholesterols and triglycerides. However, the role of FXR in foam-cell formation and atherosclerosis development remains unclear. The current study showed that the peritoneal macrophages isolated from FXR-null mice took up less oxidized LDL-cholesterol (oxLDL-C), which was accompanied by a marked reduction in CD36 expression in these cells. This result appears to be FXR-independent, as FXR was not detected in the peritoneal macrophages. To assess to what extent FXR modulates atherosclerosis development, FXR/ApoE double-null mice were generated. Female mice were used for atherosclerosis analysis. Compared to ApoE-null mice, the FXR/ApoE double-null mice were found to have less atherosclerotic lesion area in the aorta, despite a further increase in the serum cholesterols and triglycerides. Our results indicate that disruption of the FXR gene could attenuate atherosclerosis development, most likely resulting from reduced oxLDL-C uptake by macrophages. Our study cautions the use of serum lipid levels as a surrogate marker to determine the efficiency of FXR modulators in treating hyperlipidemia.

Indexed as

AnimalsApolipoproteins EAtherosclerosisBiological Transport, ActiveCholesterol, LDLCytokinesDNA-Binding ProteinsFemaleFoam CellsGene ExpressionHomeostasisIn Vitro TechniquesLipidsLipoproteins, LDLMacrophages, PeritonealMiceApolipoproteins ECholesterol, LDLCytokinesDNA-Binding ProteinsLipidsLipoproteins, LDLoxidized low density lipoproteinReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTranscription Factors

Identifiers

PMID17110163
PMCPMC1751860
OpenAlexW2130289287

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.