Molecular interactions of FGF23 and PTH in phosphate regulation.
Molecular interactions of FGF23 and PTH in phosphate regulation.
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DOI：
10.1038/ki.2014.316
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发表时间：
2014-12
影响因子：
19.6
通讯作者：
中科院分区：
文献类型：
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骨源性成纤维细胞生长因子-23 （FGF23）在全身磷酸盐转换中起重要作用。FGF23活性增加导致低磷血症，而活性降低与高磷血症相关。FGF23与klotho作为辅因子，可激活靶组织中的fgf受体，发挥其功能。然而，FGF23合成的分子调控尚不明确，近期研究发现PTH可激活核受体相关蛋白-1 (Nurr1)，诱导骨细胞中FGF23的转录。
Bone-derived fibroblast growth factor-23 (FGF23) plays an important role in systemic phosphate turnover. Increased FGF23 activity results in hypophosphatemic, while reduced activity is linked to hyperphosphatemic disorders. FGF23, together with klotho as co-factor, can activate FGF-receptors in its target tissues to exert its functions. However, molecular regulation of FGF23 synthesis is not clearly defined, and recent studies have found that PTH can activate the nuclear receptor-associated protein-1 (Nurr1) to induce FGF23 transcription in bone cells.