Evidence map›Paper›PMID 19910507›Full record

ArticleThe American journal of pathology2009

Farnesoid X receptor critically determines the fibrotic response in mice but is expressed to a low extent in human hepatic stellate cells and periductal myofibroblasts.

Peter Fickert, Andrea Fuchsbichler, Tarek Moustafa, Martin Wagner, Gernot Zollner, Emina Halilbasic, Ulrike Stöger, Marco Arrese, Margarita Pizarro, Nancy Solís and 10 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Hepatic bile acid accretion correlates with cholestatic liver injury and therapeutic response inAmerican journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  6. Review
  7. Article
  8. FXR Friend-ChIPs in the Enterohepatic System.Seminars in liver disease · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Effect of combined farnesoid X receptor agonist and angiotensin II type 1 receptor blocker on ongoing hepatic fibrosis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 5 countries.

Peter FickertLaboratory of Experimental and Molecular Hepatology, Medical University Graz, Graz, Austria.
Andrea Fuchsbichler
Tarek Moustafa
Martin Wagner
Gernot Zollner
Emina Halilbasic
Ulrike Stöger
Marco Arrese
Margarita Pizarro
Nancy Solís
Gonzalo Carrasco
Alessandra Caligiuri
Martina Sombetzki
Emil Reisinger
Oleksiy Tsybrovskyy
Kurt Zatloukal
Helmut Denk
Hartmut Jaeschke
Massimo Pinzani
Michael Trauner
Pediatrics and Genetics · USPontificia Universidad Católica de Chile · CLMedical University of Graz · ATUniversity of Rostock · DEUniversity of Kansas Medical Center · USUniversity of Florence · IT

Funding

Austrian Science Fund FWF P 18613
6 · The paper itself

Abstract

The nuclear bile acid receptor, farnesoid X receptor (FXR), may play a pivotal role in liver fibrosis. We tested the impact of genetic FXR ablation in four different mouse models. Hepatic fibrosis was induced in wild-type and FXR knock-out mice (FXR(-/-)) by CCl(4) intoxication, 3,5-diethoxycarbonyl-1,4-dihydrocollidine feeding, common bile duct ligation, or Schistosoma mansoni (S.m.)-infection. In addition, we determined nuclear receptor expression levels (FXR, pregnane X receptor (PXR), vitamin D receptor, constitutive androstane receptor (CAR), small heterodimer partner (SHP)) in mouse hepatic stellate cells (HSCs), portal myofibroblasts (MFBs), and human HSCs. Cell type-specific FXR protein expression was determined by immunohistochemistry in five mouse models and prototypic human fibrotic liver diseases. Expression of nuclear receptors was much lower in mouse and human HSCs/MFBs compared with total liver expression with the exception of vitamin D receptor. FXR protein was undetectable in mouse and human HSCs and MFBs. FXR loss had no effect in CCl(4)-intoxicated and S.m.-infected mice, but significantly decreased liver fibrosis of the biliary type (common bile duct ligation, 3,5-diethoxycarbonyl-1,4-dihydrocollidine). These data suggest that FXR loss significantly reduces fibrosis of the biliary type, but has no impact on non-cholestatic liver fibrosis. Since there is no FXR expression in HSCs and MFBs in liver fibrosis, our data indicate that these cells may not represent direct therapeutic targets for FXR ligands.

Indexed as

AnimalsFibroblastsGene ExpressionGene Expression ProfilingHepatic Duct, CommonHepatic Stellate CellsHumansImmunohistochemistryLiver CirrhosisMaleMiceMice, Inbred C57BLMice, KnockoutReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReverse Transcriptase Polymerase Chain ReactionReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, Messenger

Identifiers

PMID19910507
PMCPMC2789609
OpenAlexW1966566190

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.