Evidence map›Paper›PMID 25581518›Full record

ArticleNature medicine2015

Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction.

Mortimer Korf-Klingebiel, Marc R Reboll, Stefanie Klede, Torben Brod, Andreas Pich, Felix Polten, L Christian Napp, Johann Bauersachs, Arnold Ganser, Eva Brinkmann and 9 more

Erratum issuedOpen access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
12.7field-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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  5. Article
  6. Article
  7. Article
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  9. Article
  10. The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. The spleen in ischaemic heart disease.Nature reviews. Cardiology · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

52 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 2 institutions in 2 countries.

Mortimer Korf-Klingebiel1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Marc R Reboll1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Stefanie Klede1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Torben Brod1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Andreas PichCore Unit Mass Spectrometry and Proteomics, Institute of Toxicology, Hannover Medical School, Hannover, Germany.
Felix PoltenCore Unit Mass Spectrometry and Proteomics, Institute of Toxicology, Hannover Medical School, Hannover, Germany.
L Christian NappDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Johann BauersachsDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Arnold GanserDepartment of Hematology, Hemostasis, Oncology, and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany.
Eva Brinkmann1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Ines Reimann1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Tibor Kempf1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Hans W NiessenDepartment of Pathology and Cardiac Surgery, Institute for Cardiovascular Research, Vrije Universiteit (VU) University Medical Center, Amsterdam, the Netherlands.
Jacques MizrahiF. Hoffmann-La Roche, Pharma Research and Early Development, Basel, Switzerland.
Hans-Joachim SchönfeldF. Hoffmann-La Roche, Pharma Research and Early Development, Basel, Switzerland.
Antonio IglesiasF. Hoffmann-La Roche, Pharma Research and Early Development, Basel, Switzerland.
Maria BobadillaF. Hoffmann-La Roche, Pharma Research and Early Development, Basel, Switzerland.
Yong Wang1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Kai C Wollert1] Division of Molecular and Translational Cardiology, Hannover Medical School, Hannover, Germany. [2] Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DERoche (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paracrine-acting proteins are emerging as a central mechanism by which bone marrow cell-based therapies improve tissue repair and heart function after myocardial infarction (MI). We carried out a bioinformatic secretome analysis in bone marrow cells from patients with acute MI to identify novel secreted proteins with therapeutic potential. Functional screens revealed a secreted protein encoded by an open reading frame on chromosome 19 (C19orf10) that promotes cardiac myocyte survival and angiogenesis. We show that bone marrow-derived monocytes and macrophages produce this protein endogenously to protect and repair the heart after MI, and we named it myeloid-derived growth factor (MYDGF). Whereas Mydgf-deficient mice develop larger infarct scars and more severe contractile dysfunction compared to wild-type mice, treatment with recombinant Mydgf reduces scar size and contractile dysfunction after MI. This study is the first to assign a biological function to MYDGF, and it may serve as a prototypical example for the development of protein-based therapies for ischemic tissue repair.

Indexed as

AnimalsBone Marrow CellsCell ProliferationEndothelial CellsHEK293 CellsHumansInterleukinsMacrophagesMiceMice, KnockoutMonocytesMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacNeovascularization, PhysiologicVentricular RemodelingInterleukinsMYDGF protein, humanMydgf protein, mouse

Identifiers

PMID25581518
OpenAlexW1981573464

What OpenQuestion holds

Textmetadata
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.