Inducible

In response to chronic pressure overload, the heart undergoes pathological hypertrophy associated with adverse remodeling, fibrosis, and cardiac dysfunction. Caveolae, membrane invaginations that organize protective signaling pathways and provide a reservoir to buffer membrane tension, can ameliorate maladaptive hypertrophy. However, the factors that govern caveolae assembly in the heart are not fully understood. Here, we report that the fibroblast growth factor (FGF) homologous factor FGF13 is a negative regulator of caveolae density in cardiomyocytes. Adult mice lacking FGF13 in the heart have increased caveolae abundance in cardiomyocytes and are thereby protected from the pathological effects of chronic pressure overload. Our findings, identifying an unexpected role for FGF13, provide insight into the mechanisms underlying caveolae-mediated adaptation to cardiac stress.