Evidence map›Paper›PMID 30778201›Full record

ArticleCell death and differentiation2019

The transcription factor c-Jun/AP-1 promotes liver fibrosis during non-alcoholic steatohepatitis by regulating Osteopontin expression.

Isabel Schulien, Birgit Hockenjos, Annette Schmitt-Graeff, Markus Große Perdekamp, Marie Follo, Robert Thimme, Peter Hasselblatt

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Osteopontin in Atrial Fibrillation and Atrial Remodeling.Journal of the American Heart Association · 2026
    Review
  3. Article
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  11. bioRxiv : the preprint server for biology · 2025
    Article
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2 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

7 authors at 2 institutions in 1 country.

Isabel SchulienDepartment of Medicine II, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany.
Birgit HockenjosDepartment of Medicine II, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany.
Annette Schmitt-GraeffInstitute of Pathology, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany.
Markus Große PerdekampInstitute of Forensic Medicine, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany.
Marie FolloDepartment of Medicine I, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany.
Robert ThimmeDepartment of Medicine II, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany.
Peter HasselblattDepartment of Medicine II, Medical Center-University of Freiburg and Faculty of Medicine, University Hospital Freiburg, Freiburg, Germany. Peter.Hasselblatt@uniklinik-freiburg.de.
University of Freiburg · DEUniversity Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progression of non-alcoholic fatty liver disease (NAFLD) from steatosis to non-alcoholic steatohepatitis (NASH) is a key step of NASH pathogenesis. The AP-1 transcription factor c-Jun is an important regulator of hepatic stress responses, but its contribution to NASH pathogenesis remains poorly defined. We therefore addressed c-Jun expression in liver biopsies of patients with steatosis and NASH. The role of c-Jun during NASH pathogenesis was analyzed mechanistically in c-Jun mutant mice fed with a methionine- and choline-deficient diet (MCDD). Disease progression from steatosis to NASH in patients correlated with increased c-Jun expression in hepatocytes, while its expression in non-parenchymal liver cells (NPLCs) particularly correlated with fibrosis. Analysis of untreated and MCDD-fed mice lacking c-Jun in hepatocytes (c-Jun

Indexed as

AnimalsCell ProliferationDietDisease ProgressionHepatocytesHumansHyaluronan ReceptorsLiver CirrhosisMaleMiceMice, Inbred C57BLMice, KnockoutNon-alcoholic Fatty Liver DiseaseOsteopontinProto-Oncogene Proteins c-junRegenerationHyaluronan ReceptorsOsteopontinProto-Oncogene Proteins c-jun

Identifiers

PMID30778201
PMCPMC6748141
OpenAlexW2913699817

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.