Evidence map›Paper›PMID 26799667›Full record

ArticleOncotarget2016

TGF-β1 and TGF-β2 abundance in liver diseases of mice and men.

Anne Dropmann, Tatjana Dediulia, Katja Breitkopf-Heinlein, Hanna Korhonen, Michel Janicot, Susanne N Weber, Maria Thomas, Albrecht Piiper, Esther Bertran, Isabel Fabregat and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. New Experimental Mouse Models to Evaluate the Role of Transforming Growth Factor-Beta in Liver Tumorigenesis.Liver international : official journal of the International Association for the Study of the Liver · 2025
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  6. Review
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  17. Mig-6 Inhibits Autophagy in HCC Cell Lines by Modulating miR-193a-3p.International journal of medical sciences · 2022
    Article
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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

16 authors at 11 institutions in 3 countries.

Anne DropmannMolecular Hepatology, Department of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Tatjana DediuliaMolecular Hepatology, Department of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Katja Breitkopf-HeinleinDepartment of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Hanna KorhonenIsarna Therapeutics GmbH, Munich, Germany.
Michel JanicotIsarna Therapeutics GmbH, Munich, Germany.
Susanne N WeberDepartment of Medicine II, Saarland University Medical Center, Homburg, Germany.
Maria ThomasDr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany.
Albrecht PiiperMedizinische Klinik 1, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany.
Esther BertranBellvitge Biomedical Research Institute (IDIBELL) and University of Barcelona L'Hospitalet, Barcelona, Spain.
Isabel FabregatBellvitge Biomedical Research Institute (IDIBELL) and University of Barcelona L'Hospitalet, Barcelona, Spain.
Kerstin AbshagenInstitute for Experimental Surgery, Rostock University Medical Center, Rostock, Germany.
Jochen HessResearch Group Molecular Mechanisms of Head and Neck Tumors, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Peter AngelDivision of Signal Transduction and Growth Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Cédric CoulouarnInstitut National de la Santé et de la Recherche Médicale UMR991, University of Rennes, Pontchaillou University Hospital, Rennes, France.
Steven DooleyMolecular Hepatology, Department of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
Nadja M Meindl-BeinkerMolecular Hepatology, Department of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
University Hospital Heidelberg · DEHeidelberg University · DEIsarna Therapeutics (Germany) · DEDr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology · DEGerman Cancer Research Center · DEGoethe University Frankfurt · DEInstitut d'Investigació Biomédica de Bellvitge · ESSaarland University · DEUniversitat de Barcelona · ESUniversité de Rennes · FRUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TGF-β1 is a major player in chronic liver diseases promoting fibrogenesis and tumorigenesis through various mechanisms. The expression and function of TGF-β2 have not been investigated thoroughly in liver disease to date. In this paper, we provide evidence that TGF-β2 expression correlates with fibrogenesis and liver cancer development.Using quantitative realtime PCR and ELISA, we show that TGF-β2 mRNA expression and secretion increased in murine HSCs and hepatocytes over time in culture and were found in the human-derived HSC cell line LX-2. TGF-β2 stimulation of the LX-2 cells led to upregulation of the TGF-β receptors 1, 2, and 3, whereas TGF-β1 treatment did not alter or decrease their expression. In liver regeneration and fibrosis upon CCl4 challenge, the transient increase of TGF-β2 expression was accompanied by TGF-β1 and collagen expression. In bile duct ligation-induced fibrosis, TGF-β2 upregulation correlated with fibrotic markers and was more prominent than TGF-β1 expression. Accordingly, MDR2-KO mice showed significant TGF-β2 upregulation within 3 to 15 months but minor TGF-β1 expression changes. In 5 of 8 hepatocellular carcinoma (HCC)/hepatoblastoma cell lines, relatively high TGF-β2 expression and secretion were observed, with some cell lines even secreting more TGF-β2 than TGF-β1. TGF-β2 was also upregulated in tumors of TGFα/cMyc and DEN-treated mice. The analysis of publically available microarray data of 13 human HCC collectives revealed considerable upregulation of TGF-β2 as compared to normal liver.Our study demonstrates upregulation of TGF-β2 in liver disease and suggests TGF-β2 as a promising therapeutic target for tackling fibrosis and HCC.

Indexed as

AnimalsCell LineCell Line, TumorCells, CulturedFemaleGene Expression RegulationHepatic Stellate CellsHepatocytesHep G2 CellsHumansLiver DiseasesLiver NeoplasmsMaleMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutReceptors, Transforming Growth Factor betaTGFB1 protein, humanTransforming Growth Factor beta1Transforming Growth Factor beta2fibrosisHCCmouse modelsregenerationTGF-β isoform

Identifiers

PMID26799667
PMCPMC4991397
OpenAlexW2271556415

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.