期刊
KIDNEY INTERNATIONAL
卷 86, 期 6, 页码 1071-1074出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ki.2014.316
关键词
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资金
- NIDDK NIH HHS [R01 DK097105, DK097105] Funding Source: Medline
Bone-derived fibroblast growth factor-23 (FGF23) plays an important role in systemic phosphate turnover. Increased FGF23 activity results in hypophosphatemic disorders, while reduced activity is linked to hyperphosphatemic disorders. FGF23, together with klotho as cofactor, can activate FGF receptors in its target tissues to exert its functions. However, the molecular regulation of FGF23 synthesis is not clearly defined, and recent studies have found that parathyroid hormone (PTH) can activate the nuclear receptor-associated protein-1 (Nurr1) to induce FGF23 transcription in bone cells.
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