Evidence map›Paper›PMID 20675645›Full record

ArticleJournal of lipid research2010

Abolished synthesis of cholic acid reduces atherosclerotic development in apolipoprotein E knockout mice.

Katharina Slätis, Mats Gåfvels, Kristina Kannisto, Olga Ovchinnikova, Gabrielle Paulsson-Berne, Paolo Parini, Zhao-Yan Jiang, Gösta Eggertsen

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid 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
1.5field-weighted citation impact, top 18% 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, 55 citations in OpenAlex.

  1. Article
  2. Bile acid signaling, metabolism, and aging.Liver research (Beijing, China) · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Bile acid receptors FXR and TGR5 signaling in fatty liver diseases and therapy.American journal of physiology. Gastrointestinal and liver physiology · 2020
    Review
  14. Macrophage miR-34a Is a Key Regulator of Cholesterol Efflux and Atherosclerosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Bile Acids as Metabolic Regulators and Nutrient Sensors.Annual review of nutrition · 2019 · on this map
    Review
  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

8 authors at 1 institution in 1 country.

Katharina SlätisUnit for Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Mats Gåfvels
Kristina Kannisto
Olga Ovchinnikova
Gabrielle Paulsson-Berne
Paolo Parini
Zhao-Yan Jiang
Gösta Eggertsen
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the effects of abolished cholic acid (CA) synthesis in the ApoE knockout model [apolipoprotein E (apoE) KO],a double-knockout (DKO) mouse model was created by crossbreeding Cyp8b1 knockout mice (Cyp8b1 KO), unable to synthesize the primary bile acid CA, with apoE KO mice. After 5 months of cholesterol feeding, the development of atherosclerotic plaques in the proximal aorta was 50% less in the DKO mice compared with the apoE KO mice. This effect was associated with reduced intestinal cholesterol absorption, decreased levels of apoB-containing lipoproteins in the plasma, enhanced bile acid synthesis, reduced hepatic cholesteryl esters, and decreased hepatic activity of ACAT2. The upregulation of Cyp7a1 in DKO mice seemed primarily caused by reduced expression of the intestinal peptide FGF15. Treatment of DKO mice with the farnesoid X receptor (FXR) agonist GW4064 did not alter the intestinal cholesterol absorption, suggesting that the action of CA in this process is confined mainly to formation of intraluminal micelles and less to its ability to activate the nuclear receptor FXR. Inhibition of CA synthesis may offer a therapeutic strategy for the treatment of hyperlipidemic conditions that lead to atherosclerosis.

Indexed as

Gene Knockout TechniquesAnimalsApolipoproteins EAtherosclerosisBileCholesterolCholic AcidsIntestinal AbsorptionIsoxazolesLiverMiceMicellesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearApolipoproteins ECholesterolCholic AcidsGW 4064IsoxazolesMicellesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and Nuclear

Identifiers

PMID20675645
PMCPMC2952569
OpenAlexW2024881061

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.