Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by renal phosphate wasting, inappropriately low circulating levels of the active form of vitamin D, and skeletal abnormalities. The precise mechanisms of how excess FGF23 leads to hypophosphatemic rickets are not clear. In this issue of the
Valentin David, Myles Wolf
Vitamin D functions are regulated by a balance of 1,25(OH)2D synthesis and degradation, both systemically and locally, in vitamin D target tissues.