Evidence map›Paper›PMID 32260126›Full record

ReviewCells2020

Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives.

Natascha Roehlen, Emilie Crouchet, Thomas F Baumert

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 635 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
635citing papers in PubMed, 1 pooled it
67.7field-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

635 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,137 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Gut microbes · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. [The role of hepatocyte programmed cell death in liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. The value ofEuropean journal of nuclear medicine and molecular imaging · 2026
    Article
  19. Review
  20. Review

575 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 2 institutions in 1 country.

Natascha RoehlenUniversité de Strasbourg, 67000 Strasbourg, France.
Emilie CrouchetUniversité de Strasbourg, 67000 Strasbourg, France.
Thomas F BaumertUniversité de Strasbourg, 67000 Strasbourg, France.
Université de Strasbourg · FRHôpitaux Universitaires de Strasbourg · FR

Funding

Reverse-engineering precision liver cancer chemopreventionR01CA233794 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HOSHIDA, YUJIN · 2019 to 2023
$3.5M
Integrative genomic framework for dissecting regulatory mechanisms underlying hepatocellular carcinomaR21CA209940 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI POCHET, NATHALIE · 2017 to 2018
$402k
European Research Council 671231European Research Council 862551NCI NIH HHS R01 CA233794NCI NIH HHS R21 CA209940
6 · The paper itself

Abstract

Liver fibrosis due to viral or metabolic chronic liver diseases is a major challenge of global health. Correlating with liver disease progression, fibrosis is a key factor for liver disease outcome and risk of hepatocellular carcinoma (HCC). Despite different mechanism of primary liver injury and disease-specific cell responses, the progression of fibrotic liver disease follows shared patterns across the main liver disease etiologies. Scientific discoveries within the last decade have transformed the understanding of the mechanisms of liver fibrosis. Removal or elimination of the causative agent such as control or cure of viral infection has shown that liver fibrosis is reversible. However, reversal often occurs too slowly or too infrequent to avoid life-threatening complications particularly in advanced fibrosis. Thus, there is a huge unmet medical need for anti-fibrotic therapies to prevent liver disease progression and HCC development. However, while many anti-fibrotic candidate agents have shown robust effects in experimental animal models, their anti-fibrotic effects in clinical trials have been limited or absent. Thus, no approved therapy exists for liver fibrosis. In this review we summarize cellular drivers and molecular mechanisms of fibrogenesis in chronic liver diseases and discuss their impact for the development of urgently needed anti-fibrotic therapies.

Indexed as

AnimalsApoptosisGastrointestinal MicrobiomeHumansLiver CirrhosisModels, BiologicalOxidative StressSignal Transductionanti-fibroticsHepatic stellate cellKupffer cellliver cirrhosisliver myofibroblastPDGFTGF-β

Identifiers

PMID32260126
PMCPMC7226751
OpenAlexW3014599953

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.