Evidence map›Paper›PMID 26479335›Full record

ReviewExpert opinion on therapeutic targets2016

Therapeutic targets for cholestatic liver injury.

Benjamin L Woolbright, Hartmut Jaeschke

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Conjugated bile acid-driven CD14JHEP reports : innovation in hepatology · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Inflammation-induced cholestasis in cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2021
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Cenicriviroc, a cytokine receptor antagonist, potentiates all-trans retinoic acid in reducing liver injury in cholestatic rodents.Liver international : official journal of the International Association for the Study of the Liver · 2018
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Benjamin L Woolbrighta Department of Pharmacology , Toxicology & Therapeutics, University of Kansas Medical Center , 3901 Rainbow Blvd, MS 1018, Kansas City , KS , 66160 USA.
Hartmut Jaeschkea Department of Pharmacology , Toxicology & Therapeutics, University of Kansas Medical Center , 3901 Rainbow Blvd, MS 1018, Kansas City , KS , 66160 USA.
University of Kansas Medical Center · US

Funding

Heartland Institute for Clinical and Translational ResearchUL1TR000001 · NCATS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2012 to 2015
$13.0M
THE ROLE OF HUMAN PXR IN ANTI-TUBERCULOSIS DRUG-INDUCED LIVER INJURYP20RR021940 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI KRISHNAMURTHY, PARTHA C · 2006 to 2011
$12.1M
Nuclear Receptors in Liver Health and DiseaseP20GM103549 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2012 to 2015
$8.1M
TRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007079 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HAGENBUCH, BRUNO · 1985 to 2015
$4.1M
HEARTLAND INSTITUTE FOR CLINICAL AND TRANSLATIONAL RESEARCHUL1RR033179 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2011 to 2011
$3.2M
NEUTROPHIL-INDUCED LIVER INJURY TOXICITYR01AA012916 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2001 to 2012
$2.9M
Mitochondrial Dysfunction and Drug HepatotoxicityR01DK070195 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2005 to 2010
$1.8M
NCATS NIH HHS UL1 TR000001NCATS NIH HHS UL1TR000001NCRR NIH HHS P20 RR021940NCRR NIH HHS UL1 RR033179NCRR NIH HHS UL1RR033179NIAAA NIH HHS R01 AA012916NIAAA NIH HHS R01 AA12916NIDDK NIH HHS R01 DK070195NIEHS NIH HHS T32 ES007079NIGMS NIH HHS P20 GM103549
6 · The paper itself

Abstract

introductionCholestasis is a reduction in bile flow that occurs during numerous pathologies. Blockage of the biliary tracts results in hepatic accumulation of bile acids or their conjugate bile salts. The molecular mechanisms behind liver injury associated with cholestasis are extensively studied, but not well understood. Multiple models of obstructive cholestasis result in a significant inflammatory infiltrate at the sites of necrosis that characterize the injury. AREAS COVERED: This review will focus on direct bile acid toxicity during cholestasis, bile acid signaling processes and on the development and continuation of inflammation during cholestasis, with a focus on novel proposed molecular mediators of neutrophil recruitment. While significant progress has been made on these molecular mechanisms, a continued focus on how cholestasis and the innate immune system interact is necessary to discover targetable therapeutics that might protect the liver while leaving global immunity intact. EXPERT OPINION: While bile acid toxicity likely occurs in humans and other mammals when toxic bile acids accumulate, persistent inflammation is likely responsible for continued liver injury during obstructive cholestasis. Targeting molecular mediators of inflammation may help prevent liver injury during acute cholestasis both in murine models and human patients.

Indexed as

AnimalsBile Acids and SaltsCholestasisDisease Models, AnimalDrug DesignHumansImmunity, InnateInflammationLiver DiseasesMiceMolecular Targeted TherapyNeutrophil InfiltrationBile Acids and Saltsbile acid toxicityinflammationinnate immunityneutrophilsobstructive cholestasis

Identifiers

PMID26479335
PMCPMC4890577
OpenAlexW1852965224

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.