Evidence map›Paper›PMID 24333169›Full record

ReviewMolecular aspects of medicine2014

Clinical application of transcriptional activators of bile salt transporters.

Anna Baghdasaryan, Peter Chiba, Michael Trauner

Abstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Functional polymorphisms inOncotarget · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. [Role of farnesoid X receptor in rats with acute cholestatic hepatitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2016
    Article
  17. Nuclear Receptors as Therapeutic Targets in Liver Disease: Are We There Yet?Annual review of pharmacology and toxicology · 2016
    Review
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Anna BaghdasaryanHans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Austria; Laboratory of Experimental and Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Austria.
Peter ChibaInstitute of Medical Chemistry, Medical University of Vienna, Austria.
Michael TraunerHans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Austria. Electronic address: michael.trauner@meduniwien.ac.at.
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatobiliary bile salt (BS) transporters are critical determinants of BS homeostasis controlling intracellular concentrations of BSs and their enterohepatic circulation. Genetic or acquired dysfunction of specific transport systems causes intrahepatic and systemic retention of potentially cytotoxic BSs, which, in high concentrations, may disturb integrity of cell membranes and subcellular organelles resulting in cell death, inflammation and fibrosis. Transcriptional regulation of canalicular BS efflux through bile salt export pump (BSEP), basolateral elimination through organic solute transporters alpha and beta (OSTα/OSTβ) as well as inhibition of hepatocellular BS uptake through basolateral Na(+)-taurocholate cotransporting polypeptide (NTCP) represent critical steps in protection from hepatocellular BS overload and can be targeted therapeutically. In this article, we review the potential clinical implications of the major BS transporters BSEP, OSTα/OSTβ and NTCP in the pathogenesis of hereditary and acquired cholestatic syndromes, provide an overview on transcriptional control of these transporters by the key regulatory nuclear receptors and discuss the potential therapeutic role of novel transcriptional activators of BS transporters in cholestasis.

Indexed as

ATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily B, Member 11Bile Acids and SaltsBiological TransportCholestasisGene Expression RegulationHumansMembrane Transport ProteinsOrganic Anion Transporters, Sodium-DependentSymportersTranscriptional ActivationABCB11 protein, humanATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily B, Member 11Bile Acids and SaltsMembrane Transport ProteinsOrganic Anion Transporters, Sodium-Dependentorganic solute transporter alpha, humanSLC51B protein, humansodium-bile acid cotransporterSymporters24-norUDCA (PubChem CID: 192254)ATB-binding cassette transportersBezafibrate (PubChem CID: 39042)Budesonide (PubChem CID: 5281004)CholestasisFenofibrate (PubChem CID: 3339)FXR-450/WAY-362450 (PubChem CID: 10026128)GW4064 (PubChem CID: 9893571)Nuclear receptorsObeticholic acid/INT-747/6alpha-ethylchenodeoxycholic acid (PubChem CID: 447715)Phenobarbital (PubChem CID: 4763)Rifampicin (PubChem CID: 5381226)Ursodeoxycholic acid/UDCA/ursodiol (PubChem CID: 31401)

Identifiers

PMID24333169
PMCPMC4045202
OpenAlexW1982922137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.