Evidence map›Paper›PMID 28606651›Full record

ReviewMolecular aspects of medicine2017

Mechanisms of bile acid mediated inflammation in the liver.

Man Li, Shi-Ying Cai, James L Boyer

Open access · greenAbstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 2 pooled it
7.5field-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

112 citing papers in PubMed, 2 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cholestasis in Alcohol-Associated Liver Disease.The American journal of pathology · 2026
    Review
  15. Article
  16. Article
  17. A Review of Recent Advances in Fecal Microbiota Transplantation for the Treatment of Hepatic Encephalopathy.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  18. Article
  19. Article
  20. Article

52 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

3 authors at 1 institution in 1 country.

Man LiThe Liver Center, Yale University School of Medicine, New Haven, CT 06510, USA.
Shi-Ying CaiThe Liver Center, Yale University School of Medicine, New Haven, CT 06510, USA.
James L BoyerThe Liver Center, Yale University School of Medicine, New Haven, CT 06510, USA. Electronic address: james.boyer@yale.edu.
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI YASUKO IWAKIRI · 1986 to 2026
$31.1M
MECHANISMS OF BILE SECRETION &CHOLESTASISR37DK025636 · NIDDK · YALE UNIVERSITY · PI BOYER, JAMES LORENZEN · 1990 to 2017
$9.7M
MECHANISMS OF BILE SECRETION AND CHOLESTASISR01DK025636 · NIDDK · YALE UNIVERSITY · PI BOYER, JAMES LORENZEN · 1986 to 2007
$6.1M
NCATS NIH HHS UL1 TR001863NIDDK NIH HHS P30 DK034989NIDDK NIH HHS R01 DK025636NIDDK NIH HHS R37 DK025636
6 · The paper itself

Abstract

Bile acids are synthesized in the liver and are the major component in bile. Impaired bile flow leads to cholestasis that is characterized by elevated levels of bile acid in the liver and serum, followed by hepatocyte and biliary injury. Although the causes of cholestasis have been extensively studied, the molecular mechanisms as to how bile acids initiate liver injury remain controversial. In this chapter, we summarize recent advances in the pathogenesis of bile acid induced liver injury. These include bile acid signaling pathways in hepatocytes as well as the response of cholangiocytes and innate immune cells in the liver in both patients with cholestasis and cholestatic animal models. We focus on how bile acids trigger the production of molecular mediators of neutrophil recruitment and the role of the inflammatory response in this pathological process. These advances point to a number of novel targets where drugs might be judged to be effective therapies for cholestatic liver injury.

Indexed as

Gene Expression RegulationAnimalsBile Acids and SaltsCarrier ProteinsCholestasisCytokinesHepatocytesHumansImmunity, InnateInflammationLiverMacrophagesMembrane GlycoproteinsMiceNeutrophilsReceptor, Farnesoid X-Activatedbile acid binding proteinsBile Acids and SaltsCarrier ProteinsCytokinesGPBAR1 protein, humanMembrane GlycoproteinsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, G-Protein-CoupledBile acidsCholestatic liver injuryInflammationInnate immunityNeutrophils

Identifiers

PMID28606651
PMCPMC5662014
OpenAlexW2725385215

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.