FGF23 and myocardial infarction: [16] We found activation of β-catenin in AAV-FGF23-MI/IR mice, accompanied by upregulation of TGF-β and the deposition of collagen I/III, and these effects were antagonized by inhibition of β-catenin, suggesting that active β-catenin might promote myocardial fibrosis via TGF-β signaling in FGF23 overexpressed mice.