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Comment
. 2014 Dec;86(6):1072-4.
doi: 10.1038/ki.2014.316.

Molecular interactions of FGF23 and PTH in phosphate regulation

Beate Lanske  1 , Mohammed S Razzaque  2
Affiliations
Comment

Molecular interactions of FGF23 and PTH in phosphate regulation

Beate Lanske et al. Kidney Int. 2014 Dec.

Abstract

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 co-factor, 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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Figures

Figure 1
Figure 1
Schematic representation of currently known inducers of FGF23 production. (left) calcium (Ca++), phosphate (P), active vitamin D [1,25(OH)2D3], leptin, secreted Klotho (sKL), iron, and metabolic acidosis; (right) proposed direct stimulation of FGF23 by PTH via the Nurr1 transcription factor.
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References

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