Molecular interactions of FGF23 and PTH in phosphate regulation

被引：69

作者：

Lanske, Beate ^{[1
]}

Razzaque, Mohammed S. ^{[2
]}

机构：

[1] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immun, Boston, MA 02115 USA

[2] Forsyth Inst, Dept Appl Oral Sci, Cambridge, MA USA

来源：

KIDNEY INTERNATIONAL | 2014年 / 86卷 / 06期

关键词：

FIBROBLAST GROWTH FACTOR-23; PARATHYROID-HORMONE; HYPOPHOSPHATEMIA; KLOTHO; MICE;

D O I：

10.1038/ki.2014.316

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：1071 / 1074

页数：4

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