This study determines the effect of hepatocyte growth factor (HGF) on 
post-infarction left ventricular (LV) remodeling and cardiac function. In mice, 
on day 1 after myocardial infarction (MI), HGF (0.45 mg/kg per day) was injected 
into the tail vein for 7 days (n = 12). In the control mice (n = 12), 0.9% 
sodium chloride was injected instead of HGF. Hemodynamic data were obtained in 
vehicle treated control and HGF-treated hearts 4 weeks after the onset of MI. In 
the HGF-treated group, cardiac function was well preserved as indicated by LV 
pressure-volume relationship. These mice exhibited better LV systolic and 
diastolic function. The infarcted LV wall in HGF-treated heart was thicker as 
compared to vehicle treated group. Fibrosis and infarct size of the ventricular 
wall was significantly reduced in the HGF-treated hearts. 
5-Bromo-2'-deoxy-uridine (BrdU) and Ki67 positive cardiomyocytes were observed 
in the border area of the HGF-treated infarcted hearts. c-Met and c-kit positive 
cardiomyocytes were observed in the border area and epicardium. Angiogenesis was 
significantly enhanced in HGF-treated hearts as determined by vessel density per 
unit area. A significant reduction in apoptosis in the HGF-treated hearts was 
observed compared with control hearts, and was strongly associated with 
increased Akt activation. Treatment with HGF improved heart function through 
angiogenesis, ventricular wall thickening, and hypertrophy of cardiomyocytes. 
The antiapoptotic effect of HGF was mediated by activation of PI3-kinase/Akt 
pathway.