Beschreibung:
<jats:p>Fibroblast growth factor‐23 (FGF23) controls the homeostasis of both phosphate and vitamin D. Bone-derived FGF23 can suppress the transcription of 1α‐hydroxylase (1α(OH)ase) to reduce renal activation of vitamin D (1,25(OH)<jats:sub>2</jats:sub>D<jats:sub>3</jats:sub>). FGF23 can also activate the transcription of 24‐hydroxylase to enhance the renal degradation process of vitamin D. There is a counter-regulation for FGF23 and vitamin D; 1,25(OH)<jats:sub>2</jats:sub>D<jats:sub>3</jats:sub> induces the skeletal synthesis and the release of FGF23, while FGF23 can suppress the production of 1,25(OH)<jats:sub>2</jats:sub>D<jats:sub>3</jats:sub> by inhibiting 1α(OH)ase synthesis. Genetically ablating FGF23 activities in mice resulted in higher levels of renal 1α(OH)ase, which is also reflected in an increased level of serum 1,25(OH)<jats:sub>2</jats:sub>D<jats:sub>3</jats:sub>, while genetically ablating 1α(OH)ase activities in mice reduced the serum levels of FGF23. Similar feedback control of FGF23 and vitamin D is also detected in various human diseases. Further studies are required to understand the subcellular molecular regulation of FGF23 and vitamin D in health and disease.</jats:p>