C-terminal fragment of fibroblast growth factor 23 improves heart function in murine models of high intact fibroblast growth factor 23
Ming Chang Hu, James Reneau, Mingjun Shi, Masaya Takahashi, Gaozhi Chen, Moosa Mohammadi, Orson W. Moe
Abstract
There is a strong correlation between cardiovascular morbidity and high circulating fibroblast growth factor 23 (FGF23) levels, but causality was never proven. We used a murine chronic kidney disease (CKD) model to show that intact FGF23 (iFGF23) is pathogenic and contributes to both CKD progression and cardiomyopathy. Blockade of FGF23 signaling with a natural proteolytic product of iFGF23, C-terminal FGF23, alleviated kidney and cardiac histology, and function in three separate murine models of high endogenous FGF23.
Topics & Concepts
Fibroblast growth factorFGF1FibroblastFibroblast growth factor receptor 3Fibroblast growth factor receptorFibroblast growth factor receptor 2Basic fibroblast growth factorCell biologyGrowth factorFunction (biology)Terminal (telecommunication)ChemistryFibroblast growth factor receptor 4EndocrinologyMolecular biologyBiologyBiochemistryIn vitroComputer scienceReceptorTelecommunicationsParathyroid Disorders and TreatmentsMetabolism, Diabetes, and CancerFibroblast Growth Factor Research