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

M. Korf-Klingebiel, M.R. Reboll, S. Klede, T. Brod, A. Pich, F. Polten, L.C. Napp, J. Bauersachs, A. Ganser, E. Brinkmann, I. Reimann, T. Kempf, H.W.M. Niessen, J. Mizrahi, H.J. Schonfeld, A. Iglesias, M. Bobadilla, Y. Wang, K.C. Wollert

Research output: Contribution to journalArticleAcademicpeer-review

153 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)140-9
Number of pages10
JournalNature medicine
Issue number2
Publication statusPublished - Feb 2015


  • Animals
  • Bone Marrow Cells
  • Cell Proliferation
  • Endothelial Cells
  • HEK293 Cells
  • Humans
  • Interleukins
  • Journal Article
  • Macrophages
  • Mice
  • Mice, Knockout
  • Monocytes
  • Myocardial Infarction
  • Myocardial Reperfusion Injury
  • Myocytes, Cardiac
  • Neovascularization, Physiologic
  • Ventricular Remodeling

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