Inducible Fgf13 ablation enhances caveolae-mediated cardioprotection during cardiac pressure overload
Year: 2017
Type: article
Abstract: Significance 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.
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: bronze
Awards: Medical Scientist Training Program, George M. O'Brien Kidney Research Core Centers, G4547759372, G5001957249, Structural studies of NaV1.5 and functional implications., Calcium regulation and dysregulation of cardiac ion channels, Calmodulin regulation of Na+ channels in neurons and cardiomyocytes, Fibroblast Growth Factor Homologous Factor Modulation and Effect on Cardiac Ion Channel Trafficking, Medical Scientist Training Program Training Grant
OpenAlex ID: W2611950750