Erythropoietin: ready for prime-time cardioprotection

Trends Pharmacol Sci. 2008 May;29(5):258-67. doi: 10.1016/ Epub 2008 Mar 21.


To improve clinical outcomes in patients presenting with an acute myocardial infarction, new strategies to limit infarct size and postinfarct remodelling are warranted. Recent animal studies have revealed that erythropoietin has the potential to achieve both these goals. Even more intriguing is the possibility that erythropoietin could protect the myocardium when administered well after the onset of reperfusion. In this article we review the evidence in favour of erythropoietin-induced cardioprotection and the proposed underlying mechanisms. Inhibition of apoptosis and inflammation, as well as stimulation of neovascularization, all could contribute to cardioprotection. Activation of the reperfusion injury salvage kinase pathway at the moment of reperfusion appears to be a pivotal mechanism in the infarct size-limiting effect. Now that recent evidence has proven that erythropoietin also can protect the human heart, studies currently are being undertaken to examine the effect of administration of erythropoietin in patients presenting with an acute myocardial infarction.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Cardiotonic Agents / therapeutic use*
  • Erythropoietin / therapeutic use*
  • Humans
  • Myocardial Infarction / drug therapy
  • Myocardial Reperfusion Injury / pathology
  • Myocardial Reperfusion Injury / prevention & control*
  • Myocardium / pathology
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / pathology
  • Neovascularization, Physiologic / drug effects
  • Recombinant Proteins
  • Ventricular Remodeling / drug effects


  • Cardiotonic Agents
  • Recombinant Proteins
  • Erythropoietin