Evidence map›Paper›PMID 22221567›Full record

ReviewHPB : the official journal of the International Hepato Pancreato Biliary Association2012

Review of experimental animal models of biliary acute pancreatitis and recent advances in basic research.

Mei H Wan, Wei Huang, Diane Latawiec, Kun Jiang, David M Booth, Victoria Elliott, Rajarshi Mukherjee, Qing Xia

Open access · bronzeAbstract readReview
In one paragraph

Review in HPB : the official journal of the International Hepato Pancreato Biliary Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
5.3field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Acute pancreatitis experimental models, advantages and disadvantages.Journal of physiology and biochemistry · 2025
    Review
  3. Review
  4. Upregulation of the ERRγ-VDAC1 axis underlies the molecular pathogenesis of pancreatitis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Review
  6. Article
  7. Circulating monocytes in acute pancreatitis.Frontiers in immunology · 2022
    Review
  8. Chymase as a Novel Therapeutic Target in Acute Pancreatitis.International journal of molecular sciences · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Pathogenic mechanisms of pancreatitis.World journal of gastrointestinal pharmacology and therapeutics · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

8 authors at 4 institutions in 2 countries.

Mei H WanPancreatic Diseases Research Group, Department of Integrated Traditional and Western Medicine, West China Hospital, Sichuan University, Chengdu, China.
Wei Huang
Diane Latawiec
Kun Jiang
David M Booth
Victoria Elliott
Rajarshi Mukherjee
Qing Xia
University of Liverpool · GBWest China Hospital of Sichuan University · CNRoyal Liverpool University Hospital · GBSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute pancreatitis (AP) is a formidable disease, which, in severe forms, causes significant mortality. Biliary AP, or gallstone obstruction-associated AP, accounts for 30-50% of all clinical cases of AP. In biliary AP, pancreatic acinar cell (PAC) death (the initiating event in the disease) is believed to occur as acinar cells make contact with bile salts when bile refluxes into the pancreatic duct. Recent advances have unveiled an important receptor responsible for the major function of bile acids on acinar cells, namely, the cell surface G-protein-coupled bile acid receptor-1 (Gpbar1), located in the apical pole of the PAC. High concentrations of bile acids induce cytosolic Ca(2+) overload and inhibit mitochondrial adenosine triphosphate (ATP) production, resulting in cell injury to both PACs and pancreatic ductal epithelial cells. Various bile salts are employed to induce experimental AP, most commonly sodium taurocholate. Recent characterization of taurolithocholic acid 3-sulphate on PACs has led researchers to focus on this bile salt because of its potency in causing acinar cell injury at relatively low, sub-detergent concentrations, which strongly implicates action via the receptor Gpbar1. Improved surgical techniques have enabled the infusion of bile salts into the pancreatic duct to induce experimental biliary AP in mice, which allows the use of these transgenic animals as powerful tools. This review summarizes recent findings using transgenic mice in experimental biliary AP.

Indexed as

Acute DiseaseAnimalsBile Acids and SaltsCholestasisDisease Models, AnimalGallstonesGenotypeHumansMiceMice, TransgenicPancreatic DuctsPancreatitisPhenotypeReceptors, G-Protein-CoupledBile Acids and SaltsReceptors, G-Protein-Coupled

Identifiers

PMID22221567
PMCPMC3277048
OpenAlexW2091172771

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.