Depletion of Endothelial Prolyl Hydroxylase Domain Protein 2 and 3 Promotes Cardiomyocyte Proliferation and Prevents Ventricular Failure Induced by Myocardial Infarction

Circulation. 2019 Jul 30;140(5):440-442. doi: 10.1161/CIRCULATIONAHA.118.039276. Epub 2019 Jul 29.
No abstract available

Keywords: cell proliferation; endothelial cells; heart failure; hypoxia; myocardial infarction; myocytes, cardiac; regeneration.

Publication types

  • Letter
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Cell Proliferation / physiology*
  • Endothelium, Vascular / metabolism
  • Heart Failure / metabolism*
  • Heart Failure / prevention & control
  • Hypoxia-Inducible Factor-Proline Dioxygenases / deficiency*
  • Hypoxia-Inducible Factor-Proline Dioxygenases / genetics
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Myocardial Infarction / complications
  • Myocardial Infarction / metabolism*
  • Myocytes, Cardiac / metabolism*
  • Procollagen-Proline Dioxygenase / deficiency*
  • Procollagen-Proline Dioxygenase / genetics
  • Ventricular Dysfunction, Left / metabolism
  • Ventricular Dysfunction, Left / prevention & control

Substances

  • PHD3 protein, mouse
  • Procollagen-Proline Dioxygenase
  • Egln1 protein, mouse
  • Hypoxia-Inducible Factor-Proline Dioxygenases