Evidence map›Paper›PMID 32152325›Full record

ArticleScientific reports2020

Hypoxia sensing by hepatic stellate cells leads to VEGF-dependent angiogenesis and may contribute to accelerated liver regeneration.

Konstantin Dirscherl, Martin Schläpfer, Birgit Roth Z'graggen, Roland H Wenger, Christa Booy, Renata Flury-Frei, Rita Fatzer, Costica Aloman, Birke Bartosch, Romain Parent and 5 more

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

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  10. The Cardiohepatic Axis in Heart Failure.JACC. Basic to translational science · 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

15 authors.

Konstantin DirscherlInstitute of Physiology, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0002-5481-3547
Martin SchläpferInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Birgit Roth Z'graggenInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Roland H WengerInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Christa BooyInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Renata Flury-FreiDepartment of Pathology, Cantonal Hospital Winterthur, Zurich, Switzerland.
Rita FatzerDepartment of Pathology, Cantonal Hospital Winterthur, Zurich, Switzerland.
Costica AlomanDivision of Digestive Diseases, Rush University Medical Center, Chicago, Illinois, USA.
Birke BartoschTeam Pathogenesis of viral hepatitis UMR INSERM 1052 - CNRS 5286 Centre de recherche en cancerologie de Lyon, Lyon, France.
Romain ParentRomain Parent Inserm U1052 Team #15 - Lyon Cancer Research Center, Lyon, France.
Vartan KurtcuogluInstitute of Physiology, University of Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0003-2665-0995
Diane de ZélicourtInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Donat R SpahnInstitute of Anesthesiology, Institute of Anesthesiology, University of Zurich, University Hospital Zurich, Zurich, Switzerland.
Beatrice Beck SchimmerInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Erik SchaddeInstitute of Physiology, University of Zurich, Zurich, Switzerland. erik.schadde@uzh.ch.

Funding

Targeting mononuclear phagocytes development in alcohol induced liver damage: pathological and immunological pathwaysR01AA024762 · NIAAA · RUSH UNIVERSITY MEDICAL CENTER · PI ALOMAN, COSTICA · 2017 to 2021
$1.7M
6 · The paper itself

Abstract

Portal vein ligation (PVL) induces liver growth prior to resection. Associating liver partition and portal vein ligation (PVL plus transection=ALPPS) or the addition of the prolyl-hydroxylase inhibitor dimethyloxalylglycine (DMOG) to PVL both accelerate growth via stabilization of HIF-α subunits. This study aims at clarifying the crosstalk of hepatocytes (HC), hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC) in accelerated liver growth. In vivo, liver volume, HC proliferation, vascular density and HSC activation were assessed in PVL, ALPPS, PVL+DMOG and DMOG alone. Proliferation of HC, HSC and LSEC was determined under DMOG in vitro. Conditioned media experiments of DMOG-exposed cells were performed. ALPPS and PVL+DMOG accelerated liver growth and HC proliferation in comparison to PVL. DMOG alone did not induce HC proliferation, but led to increased vascular density, which was also observed in ALPPS and PVL+DMOG. Activated HSC were detected in ALPPS, PVL+DMOG and DMOG, again not in PVL. In vitro, DMOG had no proliferative effect on HC, but conditioned supernatant of DMOG-treated HSC induced VEGF-dependent proliferation of LSEC. Transcriptome analysis confirmed activation of proangiogenic factors in hypoxic HSC. Hypoxia signaling in HSC induces VEGF-dependent angiogenesis. HSC play a crucial role in the cellular crosstalk of rapid liver regeneration.

Indexed as

Liver RegenerationAnimalsBiomarkersCell ProliferationDisease SusceptibilityHepatic Stellate CellsHypoxiaModels, AnimalModels, BiologicalNeovascularization, PathologicRatsVascular Endothelial Growth Factor ABiomarkersVascular Endothelial Growth Factor A

Identifiers

PMID32152325
PMCPMC7062856

What OpenQuestion holds

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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.