Cardiac myocytes lose their ability for a prompt hyperplastic and hence regenerative response soon after birth, responding to increased physiological or pathological functional demand by hypertrophy. As a consequence, irreversibly damaged myocardium as occurs after myocardial infarction becomes replaced by scar tissue, the remaining myocytes adapt to the increased workload by hypertrophy, and beyond a certain potential for compensatory responses, cardiac failure ensues. It is generally accepted that interventions aimed at reducing scar size, such as stimulation of myocardial regeneration, would improve cardiac prognosis. Although very little is known about the molecular triggers of hyperplastic and/or hypertrophic growth in vivo, signaling polypeptides such as growth factors have been strongly implicated in this context. A variety of growth factors have been identified in the myocardium by us and others. 12 We have focused our attention on basic fibroblast growth factor (bFGF), since it is a potent stimulator of DNA synthesis not only in immature but also adult cardiomyocytes in culture. 3-5 Here we will provide a brief overview of current information about bFGF and its receptors as well as our own data.