Evidence map›Paper›PMID 25680861›Full record

ArticleEMBO molecular medicine2015

Hepatic stellate cell-expressed endosialin balances fibrogenesis and hepatocyte proliferation during liver damage.

Carolin Mogler, Matthias Wieland, Courtney König, Junhao Hu, Anja Runge, Claudia Korn, Eva Besemfelder, Katja Breitkopf-Heinlein, Dorde Komljenovic, Steven Dooley and 3 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  12. Diet-Regulating Microbiota and Host Immune System in Liver Disease.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Review
  15. Emerging Roles of Perivascular Mesenchymal Stem Cells in Synovial Joint Inflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  16. Article
  17. The metabolic basis of nonalcoholic steatohepatitis.Endocrinology, diabetes & metabolism · 2020
    Review
  18. Tumor angiogenesis: causes, consequences, challenges and opportunities.Cellular and molecular life sciences : CMLS · 2020
    Review
  19. Article
  20. Article
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

13 authors at 3 institutions in 1 country.

Carolin MoglerDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany Institute of Pathology Heidelberg University, Heidelberg, Germany.
Matthias WielandDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Courtney KönigDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Junhao HuDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Anja RungeDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Claudia KornDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Eva BesemfelderDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany.
Katja Breitkopf-HeinleinDepartment of Medicine II, Section Molecular Hepatology - Alcohol Associated Diseases, Medical Faculty Mannheim Heidelberg University, Heidelberg, Germany.
Dorde KomljenovicDivision of Medical Physics in Radiology, German Cancer Research Center Heidelberg, Heidelberg, Germany.
Steven DooleyDepartment of Medicine II, Section Molecular Hepatology - Alcohol Associated Diseases, Medical Faculty Mannheim Heidelberg University, Heidelberg, Germany.
Peter SchirmacherInstitute of Pathology Heidelberg University, Heidelberg, Germany German Cancer Consortium, Heidelberg, Germany.
Thomas LongerichInstitute of Pathology Heidelberg University, Heidelberg, Germany.
Hellmut G AugustinDivision of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany German Cancer Consortium, Heidelberg, Germany augustin@angiogenese.de.
Heidelberg University · DEDKFZ-ZMBH Alliance · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is a reversible wound-healing response to injury reflecting the critical balance between liver repair and scar formation. Chronic damage leads to progressive substitution of liver parenchyma by scar tissue and ultimately results in liver cirrhosis. Stromal cells (hepatic stellate cells [HSC] and endothelial cells) have been proposed to control the balance between liver fibrosis and regeneration. Here, we show that endosialin, a C-type lectin, expressed in the liver exclusively by HSC and portal fibroblasts, is upregulated in liver fibrosis in mouse and man. Chronic chemically induced liver damage resulted in reduced fibrosis and enhanced hepatocyte proliferation in endosialin-deficient (EN(KO)) mice. Correspondingly, acute-liver-damage-induced hepatocyte proliferation (partial hepatectomy) was increased in EN(KO) mice. A candidate-based screen of known regulators of hepatocyte proliferation identified insulin-like growth factor 2 (IGF2) as selectively endosialin-dependent hepatocyte mitogen. Collectively, the study establishes a critical role of HSC in the reciprocal regulation of fibrogenesis vs. hepatocyte proliferation and identifies endosialin as a therapeutic target in non-neoplastic settings.

Indexed as

Cell ProliferationAnimalsAntigens, CDAntigens, NeoplasmHepatic Stellate CellsHepatocytesHumansLiver CirrhosisLiver RegenerationMiceMice, KnockoutNeoplasm ProteinsAntigens, CDAntigens, NeoplasmCD248 protein, humanNeoplasm Proteinstumor endothelial marker 1, mouseangiocrine signalingendosialinliver fibrosisliver regeneration

Identifiers

PMID25680861
PMCPMC4364949
OpenAlexW2119085789

What OpenQuestion holds

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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.