Cardiac stem cells and early committed cells (CSCs-ECCs) express c-Met and 
insulin-like growth factor-1 (IGF-1) receptors and synthesize and secrete the 
corresponding ligands, hepatocyte growth factor (HGF) and IGF-1. HGF mobilizes 
CSCs-ECCs and IGF-1 promotes their survival and proliferation. Therefore, HGF 
and IGF-1 were injected in the hearts of infarcted mice to favor, respectively, 
the translocation of CSCs-ECCs from the surrounding myocardium to the dead 
tissue and the viability and growth of these cells within the damaged area. To 
facilitate migration and homing of CSCs-ECCs to the infarct, a growth factor 
gradient was introduced between the site of storage of primitive cells in the 
atria and the region bordering the infarct. The newly-formed myocardium 
contained arterioles, capillaries, and functionally competent myocytes that with 
time increased in size, improving ventricular performance at healing and long 
thereafter. The volume of regenerated myocytes was 2200 microm3 at 16 days after 
treatment and reached 5100 microm3 at 4 months. In this interval, nearly 20% of 
myocytes reached the adult phenotype, varying in size from 10,000 to 20,000 
microm3. Moreover, there were 43+/-13 arterioles and 155+/-48 capillaries/mm2 
myocardium at 16 days, and 31+/-6 arterioles and 390+/-56 capillaries at 4 
months. Myocardial regeneration induced increased survival and rescued animals 
with infarcts that were up to 86% of the ventricle, which are commonly fatal. In 
conclusion, the heart has an endogenous reserve of CSCs-ECCs that can be 
activated to reconstitute dead myocardium and recover cardiac function.