Evidence map›Paper›PMID 28709963›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2018

Animal models of biliary injury and altered bile acid metabolism.

Valeria Mariotti, Mario Strazzabosco, Luca Fabris, Diego F Calvisi

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 163 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Liver macrophages: development, dynamics, and functions.Cellular & molecular immunology · 2025
    Review
  11. Article
  12. Gly-βMCA modulates bile acid metabolism to reduce hepatobiliary injury inAmerican journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  13. Cell therapy for liver disorders: past, present and future.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. [Liver organoid technology and its related progress in liver disease research].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Review
  18. Article
  19. Article
  20. Article

24 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

4 authors at 3 institutions in 3 countries.

Valeria MariottiDepartment of Molecular Medicine, University of Padua, Padua, Italy.
Mario StrazzaboscoSection of Digestive Disease, Liver Center, Yale University, Yale, USA.
Luca FabrisDepartment of Molecular Medicine, University of Padua, Padua, Italy; Section of Digestive Disease, Liver Center, Yale University, Yale, USA. Electronic address: luca.fabris@unipd.it.
Diego F CalvisiInstitute of Pathology, University of Greifswald, Greifswald, Germany. Electronic address: diego.calvisi@uni-greifswald.de.
University of Padua · ITUniversitätsmedizin Greifswald · DEYale University · US

Funding

Liver disease in CF: CFTR controls innate immunity in biliary epitheliumR01DK096096 · NIDDK · YALE UNIVERSITY · PI STRAZZABOSCO, MARIO · 2013 to 2022
$4.6M
Epithelial Angiogenic Signaling in Polycystic Diseases of the LiverR01DK079005 · NIDDK · YALE UNIVERSITY · PI STRAZZABOSCO, MARIO · 2008 to 2017
$3.5M
NIDDK NIH HHS R01 DK079005NIDDK NIH HHS R01 DK096096
6 · The paper itself

Abstract

In the last 25years, a number of animal models, mainly rodents, have been generated with the goal to mimic cholestatic liver injuries and, thus, to provide in vivo tools to investigate the mechanisms of biliary repair and, eventually, to test the efficacy of innovative treatments. Despite fundamental limitations applying to these models, such as the distinct immune system and the different metabolism regulating liver homeostasis in rodents when compared to humans, multiple approaches, such as surgery (bile duct ligation), chemical-induced (3,5-diethoxycarbonyl-1,4-dihydrocollidine, DDC, α-naphthylisothiocyanate, ANIT), viral infections (Rhesus rotavirustype A, RRV-A), and genetic manipulation (Mdr2, Cftr, Pkd1, Pkd2, Prkcsh, Sec63, Pkhd1) have been developed. Overall, they have led to a range of liver phenotypes recapitulating the main features of biliary injury and altered bile acid metabolisms, such as ductular reaction, peribiliary inflammation and fibrosis, obstructive cholestasis and biliary dysgenesis. Although with a limited translability to the human setting, these mouse models have provided us with the ability to probe over time the fundamental mechanisms promoting cholestatic disease progression. Moreover, recent studies from genetically engineered mice have unveiled 'core' pathways that make the cholangiocyte a pivotal player in liver repair. In this review, we will highlight the main phenotypic features, the more interesting peculiarities and the different drawbacks of these mouse models. This article is part of a Special Issue entitled: Cholangiocytes in Health and Disease edited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.

Indexed as

AnimalsBile Acids and SaltsBile Duct DiseasesBile DuctsChronic DiseaseDisease Models, AnimalDisease ProgressionEpithelial CellsHumansLiverMiceMice, KnockoutRatsSpecies SpecificityTreatment OutcomeBile Acids and SaltsAltered bile acid metabolismBiliary injuryCholangiocyteExperimental models

Identifiers

PMID28709963
PMCPMC5764833
OpenAlexW2734346062

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.