Evidence map›Paper›PMID 25009376›Full record

ReviewWorld journal of gastroenterology2014

Fibrogenesis in alcoholic liver disease.

Hideki Fujii, Norifumi Kawada

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Implicating the cholecystokinin B receptor in liver stem cell oncogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Hepatoprotective Effect of Trehalose: Insight into Its Mechanisms of Action.Advances in experimental medicine and biology · 2021
    Article
  8. Article
  9. The Beneficial Roles of SIRT1 in Drug-Induced Liver Injury.Oxidative medicine and cellular longevity · 2019
    Review
  10. Transgenic overexpression of CTRP3 prevents alcohol-induced hepatic triglyceride accumulation.American journal of physiology. Endocrinology and metabolism · 2018
    Article
  11. Review
  12. Adipose tissue-liver axis in alcoholic liver disease.World journal of gastrointestinal pathophysiology · 2016
    Article
  13. Article
  14. Article
  15. 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

2 authors at 1 institution in 1 country.

Hideki FujiiHideki Fujii, Norifumi Kawada, Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan.
Norifumi KawadaHideki Fujii, Norifumi Kawada, Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan.
Osaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality worldwide. In developed countries, ALD is a major cause of end-stage liver disease that requires transplantation. The spectrum of ALD includes simple steatosis, alcoholic hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Alcohol abstinence is the most effective therapy for ALD. However, targeted therapies are urgently needed for patients with severe ALD (i.e., alcoholic hepatitis) or those who do not abstain from alcohol. The lack of studies and the availability of animal models that do not reflect all the features of this disease in humans inhibit the development of new drugs for ALD. In ALD-associated fibrosis, hepatic stellate cells are the principal cell type responsible for extracellular matrix production. Although the mechanisms underlying fibrosis in ALD are largely similar to those observed in other chronic liver diseases, oxidative stress, methionine metabolism abnormalities, hepatocyte apoptosis, and endotoxin lipopolysaccharides that activate Kupffer cells may play unique roles in disease-related fibrogenesis. Lipogenesis during the early stages of ALD has recently been implicated as a risk factor for the progression of cirrhosis. Other topics include osteopontin, interleukin-1 signaling, and genetic polymorphism. In this review, we discuss the basic pathogenesis of ALD and focus on liver fibrogenesis.

Indexed as

AnimalsGenetic Predisposition to DiseaseHepatic Stellate CellsHumansInflammation MediatorsKupffer CellsLipid MetabolismLiverLiver Cirrhosis, AlcoholicLiver Cirrhosis, ExperimentalOxidative StressRisk FactorsSignal TransductionInflammation MediatorsCytokineFibrosisKupffer cellOxidative stressSteatohepatitisStellate cell

Identifiers

PMID25009376
PMCPMC4081675
OpenAlexW1997268363

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.