Evidence map›Paper›PMID 23049206›Full record

ReviewWorld journal of gastroenterology2012

Novel insight into mechanisms of cholestatic liver injury.

Benjamin L Woolbright, Hartmut Jaeschke

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 196 citations in OpenAlex.

  1. Trial
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  8. HFD Exacerbates Hepatic Lipid Metabolism Disorders After Cholecystectomy by Regulating the Bile Acid and Neutrophil Recruitment.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  9. Article
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  12. Review
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  16. Review
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  18. Review
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  20. Protective Effect ofNutrients · 2022
    Article

37 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

2 authors at 1 institution in 1 country.

Benjamin L WoolbrightDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, United States.
Hartmut Jaeschke
University of Kansas Medical Center · US

Funding

TRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007079 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HAGENBUCH, BRUNO · 1985 to 2015
$4.1M
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
NIAAA NIH HHS R01 AA012916NIAAA NIH HHS R01 AA12916NIDDK NIH HHS R01 DK070195NIEHS NIH HHS T32 ES007079NIEHS NIH HHS T32 ES007079-26A2
6 · The paper itself

Abstract

Cholestasis results in a buildup of bile acids in serum and in hepatocytes. Early studies into the mechanisms of cholestatic liver injury strongly implicated bile acid-induced apoptosis as the major cause of hepatocellular injury. Recent work has focused both on the role of bile acids in cell signaling as well as the role of sterile inflammation in the pathophysiology. Advances in modern analytical methodology have allowed for more accurate measuring of bile acid concentrations in serum, liver, and bile to very low levels of detection. Interestingly, toxic bile acid levels are seemingly far lower than previously hypothesized. The initial hypothesis has been based largely upon the exposure of μmol/L concentrations of toxic bile acids and bile salts to primary hepatocytes in cell culture, the possibility that in vivo bile acid concentrations may be far lower than the observed in vitro toxicity has far reaching implications in the mechanism of injury. This review will focus on both how different bile acids and different bile acid concentrations can affect hepatocytes during cholestasis, and additionally provide insight into how these data support recent hypotheses that cholestatic liver injury may not occur through direct bile acid-induced apoptosis, but may involve largely inflammatory cell-mediated liver cell necrosis.

Indexed as

AnimalsApoptosisBile Acids and SaltsCholestasisGlycochenodeoxycholic AcidHepatocytesHumansLigationNecrosisSignal TransductionBile Acids and SaltsGlycochenodeoxycholic AcidApoptosisBile acidsBile duct ligationCholestasisInnate immunityNecrosisNeutrophils

Identifiers

PMID23049206
PMCPMC3460324
OpenAlexW2048876828

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.