FGF23　- A hormone produced by bone and has many faces

Fibroblast growth factor 23 (FGF23) was identified as an etiological factor for hypophosphatemic rickets/osteomalacia approximately a quarter-century ago. Since then, FGF23 has been shown to be a bone-derived hormone that regulates phosphate and vitamin D metabolism by binding to the α-KLOTHO-FGF receptor complex. Dysregulation of FGF23 activity results in hypophosphatemic and hyperphosphatemic disorders. Medical therapy targeting FGF23 is now available for hypophosphatemic diseases caused by FGF23 excess. Furthermore, elevated FGF23 levels have been associated with various adverse clinical outcomes, including left ventricular hypertrophy, cardiovascular events, vascular calcification, and increased mortality. Beyond its role in mineral metabolism, FGF23 has been reported to exert direct effects on other organs, contributing to conditions such as left ventricular hypertrophy, anemia, and cardiac and renal fibrosis. However, the exact mechanisms underlying these pleiotropic actions have not yet been fully elucidated. This review summarizes recent findings regarding FGF23, focusing on its classical role as a hormone and its broader effects as a humoral factor on other organs.