A basic study of Klotho as a local factor of hard tissue reproduction

Klotho与FGF23-FGF受体（FGFR）形成复合物，这是fgf23介导的矿化缺陷所必需的，而Klotho在骨中不表达。因此，我们利用体外大鼠颅骨来源的成骨细胞/骨细胞和体内Klotho突变小鼠，验证了Klotho的细胞外结构域（被截断并分泌到循环中）有助于FGF23在骨中的作用的假设。总之，我们证明了KLe在骨中与FGF23-FGFR形成复合物，通过fgf23依赖性ERK信号通路导致低矿化。

Klotho forms a complex with FGF23-FGF receptor (FGFR), which is necessary for FGF23-mediated mineralization defects, whereas Klotho is not expressed in bone. We therefore tested the hypothesis that the extracellular domain of Klotho (KLe), which is truncated and secreted into the circulation, contributes to FGF23 action in bone using rat calvaria-derived osteoblasts/osteocytes in vitro and Klotho-mutant mice in vivo. In conclusion, we demonstrated that KLe forms a complex with FGF23-FGFR in bone, resulting in hypomineralization through an FGF23-dependent ERK signaling pathway.