Hsp90 Inhibitor Attenuates the Development of Pathophysiological Cardiac Fibrosis in Mouse Hypertrophy via Suppression of the Calcineurin-NFAT and c-Raf-Erk Pathways.

In the previous study, we showed that an Hsp90 inhibitor, 17-(allylamino)-17-demethoxygeldanamycin (17-AAG), attenuates hypertrophic remodeling of cardiomyocytes during the development of heart failure. In this present study, we investigated the effects of 17-AAG on cardiac fibrosis during the development of heart failure. We used pressure-loaded cardiac hypertrophic mice prepared by constriction of the transverse aorta (TAC), which induces significant cardiac fibrosis without scar tissue.