Evidence map›Paper›PMID 31969775›Full record

ReviewWorld journal of gastroenterology2020

Inflammation and fibrosis in chronic liver diseases including non-alcoholic fatty liver disease and hepatitis C.

Sudeep Tanwar, Freya Rhodes, Ankur Srivastava, Paul M Trembling, William M Rosenberg

Open access · greenAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 4 pooled it
20.5field-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

119 citing papers in PubMed, 4 syntheses or guidelines pooled it, 233 citations in OpenAlex.

  1. Pooled it
  2. Advances in pathogenesis of preeclampsia.Archives of gynecology and obstetrics · 2024
    Pooled it
  3. Pooled it
  4. Pooled it
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  8. Review
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  14. Effects of Melatonin andAntioxidants (Basel, Switzerland) · 2026
    Article
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  16. Article
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  19. Review
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59 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

5 authors at 1 institution in 1 country.

Sudeep TanwarUCL Institute for Liver and Digestive Health, Division of Medicine, University College London, Royal Free Campus, Hampstead, London NW3 2PF United Kingdom.
Freya RhodesUCL Institute for Liver and Digestive Health, Division of Medicine, University College London, Royal Free Campus, Hampstead, London NW3 2PF United Kingdom.
Ankur SrivastavaUCL Institute for Liver and Digestive Health, Division of Medicine, University College London, Royal Free Campus, Hampstead, London NW3 2PF United Kingdom.
Paul M TremblingUCL Institute for Liver and Digestive Health, Division of Medicine, University College London, Royal Free Campus, Hampstead, London NW3 2PF United Kingdom.
William M RosenbergUCL Institute for Liver and Digestive Health, Division of Medicine, University College London, Royal Free Campus, Hampstead, London NW3 2PF United Kingdom.
Royal Free London NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At present chronic liver disease (CLD), the third commonest cause of premature death in the United Kingdom is detected late, when interventions are ineffective, resulting in considerable morbidity and mortality. Injury to the liver, the largest solid organ in the body, leads to a cascade of inflammatory events. Chronic inflammation leads to the activation of hepatic stellate cells that undergo trans-differentiation to become myofibroblasts, the main extra-cellular matrix producing cells in the liver; over time increased extra-cellular matrix production results in the formation of liver fibrosis. Although fibrogenesis may be viewed as having evolved as a "wound healing" process that preserves tissue integrity, sustained chronic fibrosis can become pathogenic culminating in CLD, cirrhosis and its associated complications. As the reference standard for detecting liver fibrosis, liver biopsy, is invasive and has an associated morbidity, the diagnostic assessment of CLD by non-invasive testing is attractive. Accordingly, in this review the mechanisms by which liver inflammation and fibrosis develop in chronic liver diseases are explored to identify appropriate and meaningful diagnostic targets for clinical practice. Due to differing disease prevalence and treatment efficacy, disease specific diagnostic targets are required to optimally manage individual CLDs such as non-alcoholic fatty liver disease and chronic hepatitis C infection. To facilitate this, a review of the pathogenesis of both conditions is also conducted. Finally, the evidence for hepatic fibrosis regression and the mechanisms by which this occurs are discussed, including the current use of antifibrotic therapy.

Indexed as

Adaptive ImmunityAnimalsAntiviral AgentsBiopsyDisease Models, AnimalDisease ProgressionDrug RepositioningHepatic Stellate CellsHepatitis C, ChronicHepatocytesHumansImmunity, InnateImmunologic FactorsInflammasomesLipogenesisLiverAntiviral AgentsImmunologic FactorsInflammasomesReceptors, Pattern RecognitionAnti-fibroticBiomarkerChronic hepatitis CChronic liver diseaseCirrhosisFibrosisLiver inflammationNon-alcoholic fatty liver disease

Identifiers

PMID31969775
PMCPMC6962431
OpenAlexW2999506325

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.