Fibroblast Growth Factor 23
The most frequent inherited renal phosphate-wasting disease in humans is X-linked hypophosphatemia (XLH). The murine homolog of this disease is Hyp (hypophosphatemia). XLH patients and Hyp mice lose phosphate via the urine, and show impaired bone mineralization as a consequence of hypophosphatemia and alterations in the organic bone matrix. Kidney transplantation and parabiosis experiments in Hyp mice had suggested in the late 1980s that the renal phosphate wasting is not caused by defects in the kidney, but rather by some unknown factor circulating in the blood (Meyer et al. 1989). Since all at that time known endocrine regulators of phosphate metabolism could be ruled out as disease-causing factors, the putative phosphaturic substance circulating in the blood stream was named “phosphatonin.” However, it should take more than 10 years to find this phosphaturic factor, which turned out to be fibroblast growth factor 23 (FGF23). FGF23 was discovered...
This work was supported by a grant from the Austrian Science Fund (FWF 24186-B21) to R.G.E.
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