Evidence map›Paper›PMID 37280200›Full record

ArticleNature communications2023

Colitis ameliorates cholestatic liver disease via suppression of bile acid synthesis.

Wenfang Gui, Mikal Jacob Hole, Antonio Molinaro, Karolina Edlund, Kristin K Jørgensen, Huan Su, Brigitte Begher-Tibbe, Nikolaus Gaßler, Carolin V Schneider, Uthayakumar Muthukumarasamy and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
10.6field-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

23 citing papers in PubMed, 52 citations in OpenAlex.

  1. Bile acid signaling in health and disease.Molecular biomedicine · 2026
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  14. Resident CD24Acta biochimica et biophysica Sinica · 2025
    Article
  15. Bile acids as therapeutic agents.Frontiers in pharmacology · 2025
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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

21 authors at 8 institutions in 5 countries.

Wenfang GuiDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.ORCID 0009-0006-2317-6959
Mikal Jacob HoleNorwegian PSC Research Center, Section of Gastroenterology and Research Institute of Internal Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital and University of Oslo, Oslo, Norway.
Antonio MolinaroDepartment of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
Karolina EdlundLeibniz Research Centre for Working Environment and Human Factors, Technical University Dortmund, Dortmund, 44139, Germany.
Kristin K JørgensenNorwegian PSC Research Center, Department of Transplantation Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Huan SuDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.
Brigitte Begher-TibbeLeibniz Research Centre for Working Environment and Human Factors, Technical University Dortmund, Dortmund, 44139, Germany.
Nikolaus GaßlerInstitute for Legal Medicine, Section Pathology, University Hospital, Jena, 07747, Germany.
Carolin V SchneiderDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.
Uthayakumar MuthukumarasamyHelmholtz Centre for Infection Research, Braunschweig, Germany and Centre for Individualised Infection Medicine (CiiM), a joint venture between the Helmholtz-Centre for Infection Research (HZI) and the Hannover Medical School (MHH), Hannover, 97080, Germany.
Antje MohsDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.ORCID 0000-0001-5937-0696
Lijun LiaoDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.
Julius JaegerDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.ORCID 0000-0002-1122-5331
Christian J MertensDepartment of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany.ORCID 0000-0001-7303-2650
Ina BergheimDepartment of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, A-1090, Austria.ORCID 0000-0002-3356-4115
Till StrowigHelmholtz Centre for Infection Research, Braunschweig, Germany and Centre for Individualised Infection Medicine (CiiM), a joint venture between the Helmholtz-Centre for Infection Research (HZI) and the Hannover Medical School (MHH), Hannover, 97080, Germany.ORCID 0000-0003-0185-1459
Jan G HengstlerLeibniz Research Centre for Working Environment and Human Factors, Technical University Dortmund, Dortmund, 44139, Germany.ORCID 0000-0002-1427-5246
Johannes R HovNorwegian PSC Research Center, Section of Gastroenterology and Research Institute of Internal Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital and University of Oslo, Oslo, Norway.ORCID 0000-0002-5900-8096
Hanns-Ulrich MarschallDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden.ORCID 0000-0001-7347-3085
Christian Trautwein *Department of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany. ctrautwein@ukaachen.de.ORCID 0000-0003-2762-8247
Kai Markus Schneider *Department of Medicine III, University Hospital RWTH Aachen, Aachen, 52074, Germany. kmschneider@ukaachen.de.ORCID 0000-0002-0047-3794
RWTH Aachen University · DEOslo University Hospital · NOTU Dortmund University · DEMedizinische Hochschule Hannover · DEUniversitätsklinikum Aachen · DEShanghai East Hospital · CNUniversity of Gothenburg · SEUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterized by chronic inflammation and progressive fibrosis of the biliary tree. The majority of PSC patients suffer from concomitant inflammatory bowel disease (IBD), which has been suggested to promote disease development and progression. However, the molecular mechanisms by which intestinal inflammation may aggravate cholestatic liver disease remain incompletely understood. Here, we employ an IBD-PSC mouse model to investigate the impact of colitis on bile acid metabolism and cholestatic liver injury. Unexpectedly, intestinal inflammation and barrier impairment improve acute cholestatic liver injury and result in reduced liver fibrosis in a chronic colitis model. This phenotype is independent of colitis-induced alterations of microbial bile acid metabolism but mediated via hepatocellular NF-κB activation by lipopolysaccharide (LPS), which suppresses bile acid metabolism in-vitro and in-vivo. This study identifies a colitis-triggered protective circuit suppressing cholestatic liver disease and encourages multi-organ treatment strategies for PSC.

Indexed as

Cholangitis, SclerosingCholestasisColitisInflammatory Bowel DiseasesLiver DiseasesAnimalsBile Acids and SaltsInflammationMiceBile Acids and Salts

Identifiers

PMID37280200
PMCPMC10244448
OpenAlexW4379598812

What OpenQuestion holds

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LicenceCC BY
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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.