Erythropoietin (EPO) has been suggested to have a cardioprotective effect 
against ischemia. The purpose of this study was to examine the effects of EPO on 
cardiac remodeling after myocardial infarction (MI). MI was induced by ligation 
of the coronary artery in Wistar rats. The rats with MI were randomly divided 
into untreated MI and two EPO-treated MI groups. EPO was administered 
subcutaneously by injection once a day for 4 days after MI at 5000 U/kg or 3 
times a week for 4 weeks at 1000 U/kg. Five days after MI, EPO prevented the 
increase in activated caspase 3, matrix metalloproteinase-2, and transcriptional 
activation of activator protein-1 in non-infarcted myocardium. Four weeks after 
MI, left ventricular weight, left ventricular end-diastolic pressure, and left 
ventricular dimension were increased, and ejection fraction and E wave 
deceleration time were decreased. EPO significantly attenuated this ventricular 
remodeling and systolic and diastolic dysfunction. In addition, EPO 
significantly attenuated the interstitial fibrosis and remodeling-related gene 
expression in non-infarcted myocardium. Furthermore, EPO significantly enhanced 
angiogenesis and reduced apoptotic cell death in peri-infarcted myocardium. In 
conclusion, when administered after MI, EPO prevents cardiac remodeling and 
improves ventricular function with enhanced angiogenesis and reduced apoptosis.