摘要INTRODUCTIONMaintenance of normal mineral balance is necessary for proper structure of the skeleton, which also provides the long-term provision of phosphate and calcium as substrates for cellular use. Fibroblast growth factor-23 (FGF23) is a key factor involved in the endocrine axis regulating mineral ion handling. In this regard, FGF23 is secreted from bone cells (osteoblasts and osteocytes) in response to elevated circulating levels of phosphate or 1,25-dihydroxyvitamin D (1,25D). In the kidney, FGF23 regulates serum phosphate by reducing proximal tubule sodium-phosphate transporter content via downstream signaling initiated by binding to FGF receptors (FGFRs) and its co-receptor αKlotho.1 These interactions reduce blood 1,25D through downregulation of the 1,25D anabolic 1α-hydroxylase enzyme (Cyp27b1) and upregula-tion of the catabolic 24-hydroxylase (Cyp24a1).2 In addition to factors involved in mineral metabolism, other regulators of FGF23 production have been identified that tie systemic oxygenation to bone, including hypoxia and iron deficiency anemia.3–4 Osteo-cytes, which comprise over 95％of bone cells, reside in a hypoxic environment, with oxygen tensions below 10％(cortical bone pO2