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How do we sense phosphate to regulate serum phosphate level?

Abnormal phosphate levels result in several pathological conditions such as rickets/osteomalacia and ectopic calcification indicating that there must be a system that regulates phosphate level within a narrow range. FGF23 has been shown to be an essential hormone regulating serum phosphate level. FG...

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Bibliographic Details
Published in:Journal of bone and mineral metabolism 2020, Vol.38 (1), p.1-6
Main Authors: Fukumoto, Seiji, Takashi, Yuichi, Tsoumpra, Maria K., Sawatsubashi, Shun, Matsumoto, Toshio
Format: Article
Language:English
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Summary:Abnormal phosphate levels result in several pathological conditions such as rickets/osteomalacia and ectopic calcification indicating that there must be a system that regulates phosphate level within a narrow range. FGF23 has been shown to be an essential hormone regulating serum phosphate level. FGF23 binds to Klotho-FGF receptor complex to reduce serum phosphate level. Several reports suggested that FGF receptor is involved in the regulation of FGF23 production. It has been also shown that high extracellular phosphate can activate several intracellular signaling pathways. However, it has been unclear whether and how phosphate regulates FGF23 production in vivo. Our recent results indicate that high extracellular phosphate directly activates FGF receptor 1 and the downstream intracellular signaling enhances FGF23 production. Thus, there is a negative feedback system for the regulation of serum phosphate level involving FGF receptor and FGF23. We propose that FGF receptor works at least as one of phosphate sensors in the maintenance of serum phosphate level.
ISSN:0914-8779
1435-5604
DOI:10.1007/s00774-019-01066-0