IGF-1 Overexpression rescues the failing heart.

Congestive heart failure (CHF) is a syndrome affecting nearly 5 million Americans with 550 000 new cases diagnosed annually. Despite recent advances in pharmacological therapy, the enormity of the clinical problem has stimulated cardiovascular scientists to test a variety of new and provocative hypotheses that may ultimately prove useful in CHF prevention and treatment. One such novel approach is addressed by Welch et al1 in this issue of Circulation Research. They tested the hypothesis that insulin-like growth factor-1 (IGF-1), a peptide growth factor involved in cardiomyocyte proliferation, differentiation, and cell survival, can positively affect CHF progression in a transgenic mouse model of dilated cardiomyopathy. The study provides new and important information about the cellular mechanisms leading to ventricular remodeling and also adds to the current controversy regarding the roles of cardiomyocyte apoptosis and regeneration in the pathogenesis of CHF.