The molecular chaperone Hsp90 is involved in the stabilization of client proteins. Hsp90 client proteins are diverse and contain many signal transmitters including protein kinases. Cardiac remodeling such as cardiac hypertrophy is well known to play a role in the development of chronic heart failure following myocardial infarction. Cardiac remodeling is regulated by many signaling pathways, and c-Raf that is also an Hsp90 client protein is a signaling molecule involved in cardiac hypertrophy. Therefore, to clarify the roles of Hsp90 and its clients in progression to the chronic heart failure, we examined effects of Hsp90 inhibitor on the signal transducers in the development of chronic heart failure following myocardial infarction in animal models. Treatment of the animals with Hsp90 inhibitor resulted in a suppression of cardiac remodeling and a preservation of cardiac pump function after myocardial infarction. Furthermore, c-Raf and phosphorylated Erk contents were decreased by an administration of Hsp90 inhibitor. These results suggest that Hsp90 contributes to cardiac hypertrophy in the development of heart failure via regulating c-Raf.