To test this hypothesis, we provided both in vitro and in vivo evidence that overexpression of FGF23 promotes proliferation of cardiac fibroblasts and increases myocardial fibrosis in mice with ischemia/reperfusion (IR) or permanent myocardial infarction (MI) through activation of β-catenin and upregulation of TGF-β. Here, FGF23 is linked to myocardial infarction.