We found upregulation of renal active-β-catenin expression in CRS mice with myocardial overexpression of FGF23, which was accompanied by upregulation of TGF-β and deposition of collagen I. FGF23 is known to inhibit renal synthesis of active vitamin D, while treatment with vitamin D analogs can suppress upregulation of active-β-catenin, TGF-β1, and collagens in chronic kidney disease [55], supporting our finding that excess FGF23 upregulates active-β-catenin, TGF-β1, and collagens in CRS mice. Here, FGF23 is linked to chronic kidney disease.