Evidence map›Paper›PMID 20422500›Full record

ReviewSeminars in liver disease2010

The role of inflammation in cholestasis: clinical and basic aspects.

Astrid Kosters, Saul J Karpen

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in liver disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

85 citing papers in PubMed, 203 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Mechanistic insights into the liver-brain axis during chronic liver disease.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Intrahepatic cholestasis of pregnancy.Nature reviews. Disease primers · 2025
    Review
  16. Article
  17. Review
  18. Mechanisms of sepsis-induced acute liver injury: a comprehensive review.Frontiers in cellular and infection microbiology · 2025
    Review
  19. Article
  20. Article

25 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.

Astrid KostersTexas Children's Liver Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA.
Saul J Karpen
Baylor College of Medicine · US

Funding

MOLECULAR REGULATION OF HEPATIC TRANSPORTERSR01DK056239 · NIDDK · YALE UNIVERSITY · PI KARPEN, SAUL J. · 1999 to 2017
$4.8M
NIDDK NIH HHS R01 DK056239
6 · The paper itself

Abstract

Hepatobiliary transport systems are essential for the uptake and excretion of a variety of compounds including bile acids. Disruption and dysregulation of this excretory pathway result in cholestasis, leading to the intrahepatic accumulation of bile acids and other toxic compounds with progression of liver pathology. Cholestasis induced by inflammation is a common complication in patients with extrahepatic infections or inflammatory processes, generally referred to as sepsis-associated cholestasis. Microbial products, including endotoxin, induce signaling pathways within hepatocytes either directly, or through activation of proinflammatory cytokines, leading to rapid and profound reductions in bile flow. The expression and function of key hepatobiliary transporters are suppressed in response to inflammatory signaling. These proinflammatory signaling cascades lead to repressed expression and activity of a large number of nuclear transcriptional regulators, many of which are essential for maintenance of hepatobiliary transporter gene expression. Interestingly, recently discovered molecular crosstalk between bile acid activated nuclear receptors and proinflammatory nuclear mediators may provide new means of understanding adaptive processes within liver. Inflammation-induced cholestasis and the effects of retained molecules in cholestasis on inflammatory signals are interwoven in the liver, providing potential opportunities for research and therapeutics.

Indexed as

Bile Acids and SaltsCholestasisDisease ProgressionHumansInfant, NewbornInflammationJaundice, NeonatalLiverParenteral Nutrition, TotalReceptor Cross-TalkReceptors, Cytoplasmic and NuclearSepsisBile Acids and SaltsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID20422500
PMCPMC3746018
OpenAlexW2015162068

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.