Evidence map›Paper›PMID 38316785›Full record

ArticleNature communications2024

Identification of myeloid-derived growth factor as a mechanically-induced, growth-promoting angiocrine signal for human hepatocytes.

Linda Große-Segerath, Paula Follert, Kristina Behnke, Julia Ettich, Tobias Buschmann, Philip Kirschner, Sonja Hartwig, Stefan Lehr, Mortimer Korf-Klingebiel, Daniel Eberhard and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Mechanical Loading Induces Distinct and Shared Responses in Endothelial and Muscle Cells and Reveals Exercise-Like Molecular Profiles.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  8. Blood flow-induced angiocrine signals promote organ growth and regeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  9. Review
  10. Review
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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

18 authors at 5 institutions in 1 country.

Linda Große-Segerath *Heinrich Heine University Düsseldorf, Faculty of Mathematics and Natural Sciences, Institute of Metabolic Physiology, 40225, Düsseldorf, Germany.
Paula Follert *Heinrich Heine University Düsseldorf, Faculty of Mathematics and Natural Sciences, Institute of Metabolic Physiology, 40225, Düsseldorf, Germany.
Kristina BehnkeInstitute of Biochemistry and Molecular Biology II, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Julia EttichInstitute of Biochemistry and Molecular Biology II, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Tobias BuschmannInstitute for Molecular Medicine III, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.ORCID 0000-0001-9192-9445
Philip KirschnerHeinrich Heine University Düsseldorf, Faculty of Mathematics and Natural Sciences, Institute of Metabolic Physiology, 40225, Düsseldorf, Germany.ORCID 0000-0002-6711-5959
Sonja HartwigGerman Center for Diabetes Research (DZD e.V.), Helmholtz Zentrum München, 85764, Neuherberg, Germany.ORCID 0000-0002-5225-6804
Stefan LehrGerman Center for Diabetes Research (DZD e.V.), Helmholtz Zentrum München, 85764, Neuherberg, Germany.ORCID 0000-0003-3971-357X
Mortimer Korf-KlingebielDivision of Molecular and Translational Cardiology, Department of Cardiology and Angiology, Hannover Medical School, 30625, Hannover, Germany.
Daniel EberhardHeinrich Heine University Düsseldorf, Faculty of Mathematics and Natural Sciences, Institute of Metabolic Physiology, 40225, Düsseldorf, Germany.
Nadja Lehwald-TywuschikDepartment of General, Visceral, Thorax and Pediatric Surgery, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Hadi Al-HasaniGerman Center for Diabetes Research (DZD e.V.), Helmholtz Zentrum München, 85764, Neuherberg, Germany.
Wolfram Trudo KnoefelDepartment of General, Visceral, Thorax and Pediatric Surgery, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Stefan HeinrichDepartment of General, Visceral and Transplantation Surgery, University Hospital Center Mainz, 55131, Mainz, Germany.
Bodo LevkauInstitute for Molecular Medicine III, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.ORCID 0000-0002-0005-125X
Kai C WollertDivision of Molecular and Translational Cardiology, Department of Cardiology and Angiology, Hannover Medical School, 30625, Hannover, Germany.ORCID 0000-0002-4890-4450
Jürgen SchellerInstitute of Biochemistry and Molecular Biology II, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Eckhard LammertHeinrich Heine University Düsseldorf, Faculty of Mathematics and Natural Sciences, Institute of Metabolic Physiology, 40225, Düsseldorf, Germany. lammert@hhu.de.ORCID 0000-0002-9844-8000
Düsseldorf University Hospital · DEHelmholtz Zentrum München · DEHeinrich Heine University Düsseldorf · DEMedizinische Hochschule Hannover · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, we have shown that after partial hepatectomy (PHx), an increased hepatic blood flow initiates liver growth in mice by vasodilation and mechanically-triggered release of angiocrine signals. Here, we use mass spectrometry to identify a mechanically-induced angiocrine signal in human hepatic endothelial cells, that is, myeloid-derived growth factor (MYDGF). We show that it induces proliferation and promotes survival of primary human hepatocytes derived from different donors in two-dimensional cell culture, via activation of mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3). MYDGF also enhances proliferation of human hepatocytes in three-dimensional organoids. In vivo, genetic deletion of MYDGF decreases hepatocyte proliferation in the regenerating mouse liver after PHx; conversely, adeno-associated viral delivery of MYDGF increases hepatocyte proliferation and MAPK signaling after PHx. We conclude that MYDGF represents a mechanically-induced angiocrine signal and that it triggers growth of, and provides protection to, primary mouse and human hepatocytes.

Indexed as

Endothelial CellsInterleukinsLiver RegenerationAnimalsCell ProliferationHepatectomyHepatocytesHumansLiverMiceMitogen-Activated Protein KinasesInterleukinsMitogen-Activated Protein KinasesMYDGF protein, human

Identifiers

PMID38316785
PMCPMC10844291
OpenAlexW4391543699

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.