Regulatory mechanisms of mineral homeostasis by FGF23

成纤维细胞生长因子23（FGF 23）是一种由骨产生的激素，主要作用于肾脏，降低血清磷酸盐水平。已经表明，FGF 23的过度作用引起几种低磷酸盐血症性佝偻病/骨软化症。此外，循环FGF 23水平在慢性肾病（CKD）患者中显示较高。然而，尚不清楚是什么诱导了低磷酸盐血症性佝偻病/骨软化症患者中FGF 23的过度作用，以及CKD患者中高FGF 23是否在磷酸盐代谢中具有任何显著作用。我们已经报道了几个基因的突变通过增加血清FGF 23水平引起低磷血症性佝偻病，并且抑制FGF 23活性可以改善低磷血症性佝偻病模型小鼠的疾病状态。此外，CKD患者中增加的FGF 23已被证明可预防高磷酸盐血症的发展。这些结果表明，FGf 23在健康人和磷酸盐水平异常的患者的磷酸盐代谢中发挥着关键作用。

Fibroblast growth factor 23(FGF23) is a hormone that is produced by bone and lowers serum phosphate level by acting mainly on kidney. It has been shown that excess actions of FGF23 cause several kinds of hypophosphatemic rickets/osteomalacia. In addition circulatory FGF23 level was shown to be high in patients with chronic kidney disease(CKD). However, it has been unknown what induces excess actions of FGF23 in patients with hypophosphatemic rickets/osteomalacia and whether high FGF23 in patients with CKD has any significant role in phosphate metabolism. We have reported that mutations in several genes cause hypophosphatemic rickets by increasing serum level of FGF23 and the inhibition of FGF23 activity can improve disease status in a model mouse of hypophosphatemic rickets. Furthermore, increased FGF23 in patients with CKD has been shown to work to prevent the development of hyperphosphatemia. These results indicate that FGf23 has a pivotal role in phosphate metabolism both in healthy people and patients with abnormal phosphate levels.