Fibroblast Growth Factor 23 Is a Promissing Marker of Myocardial Pathology

Abstract

Purpose Fibroblast growth factor 23 (FGF23) is a main bone hormone responsible for the phosphate homeostasis. Moreover it is a good biomarker of chronic kidney disease. The only experimental report concerning FGF23 in the heart displayed its toxic effect on mice myocardium resulted in hypertrophy after intravenous injection of FGF23. However, there is no notification of FGF23 heart expression. Currently we observed that isolated neonatal as well as adult cardiomyocytes (CM) are able to produce FGF23 in stress conditions, but data in vivo are missing. Methods and Materials For this purpose we studied heart explants of 10 patients suffering from ischemic cardiomyopathy (ICM), 14 patients with dilated cardiomyopathy (DCM) and 12 patients with myocarditis (Myo). 2 healthy donor hearts (which were not used for transplantation) served as controls. In addition we used animal models: wild-type mice with myocardial infarction (WT-MI) induced by LAD ligation and transgenic mice with a cardiac restricted overexpression of monocyte chemotactic protein (MCP1) as a model of chronic inflammation. Results We firstly detected FGF23 positive CM in vivo. They were localized in diseased myocardium as isolated cells or in groups showing week or marked cross-striation. The number of FGF23 expressing CM was increased 14.8 fold in patients with ICM, 12.3 fold in DCM patients and 13.5 fold in patients with Myo in comparison with controls (p Conclusions For the first time we demonstrated FGF 23 expression in myocardium of patients with heart failure and in mice models. An increased activity of FGF23 and its receptor FGFR1c in stress conditions characterizes the FGF23 as a promising diagnostic and prognostic biomarker of cardiac pathology.