Abstract
Fibroblast growth factor 23 (FGF23) decreases serum phosphate by inhibiting proximal tubular phosphate reabsorption and intestinal phosphate absorption through the reduction of serum 1,25-dihydroxyvitamin D [1,25 (OH) (2)D] levels. Excessive actions of FGF23 cause hypophosphatemic diseases with impaired mineralization of bone. On the other hand, impaired actions of FGF23 result in hyperphosphatemic familial tumoral calcinosis characterized by hyperphosphatemia and high 1,25 (OH) (2)D levels. Ectopic calcification around large joints and in blood vessels can be observed in patients with this disease. Therefore, FGF23 plays essential roles in the regulation of bone mineralization and prevention of ectopic calcification.
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