Augmented Cardiac Hypertrophy in Response to Pressure Overload in Mice Lacking the Prostaglandin I ₂ Receptor

Abstract

IP plays a suppressive role in the development of pressure overload-induced cardiac hypertrophy via the inhibition of both cardiomyocyte hypertrophy and cardiac fibrosis. Both effects have been suggested as originating from the action on noncardiomyocytes rather than cardiomyocytes.