Molecular interactions of FGF23 and PTH in phosphate regulation.
Level V
Where this comes from
- Record sourced from PubMed, PMID 25427080.
- Also identified by DOI 10.1038/ki.2014.316 and PMC identifier 4246422.
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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.
Medical subject headings
- Fibroblast Growth Factors
- Nuclear Receptor Subfamily 4, Group A, Member 2
- Parathyroid Hormone
- RNA, Messenger
- Transcription, Genetic