Fgf23, or fibroblast growth factor 23, is a phosphotropic hormone crucial for maintaining phosphate homeostasis [1,2]. It belongs to a subfamily of endocrine FGFs with conserved functions across species. Fgf23 reduces serum phosphate levels by inhibiting 1,25-dihydroxyvitamin D synthesis, suppressing intestinal phosphate absorption, and downregulating renal phosphate transporters NPT2a and NPT2c [1]. It binds to the FGFR1c-α-KLOTHO complex, activating the FRS2/RAS/RAF/MEK/ERK1/2 pathway [1].

Fgf23 deficiency in mouse models causes hyperphosphatemia and ectopic calcifications, while excess leads to hypophosphatemia and skeletal defects [2]. In the context of chronic kidney disease (CKD), elevated Fgf23 levels are associated with increased cardiovascular disease and mortality, and Fgf23 may contribute to cardiac hypertrophy and anemia development [3,4].

In conclusion, Fgf23 is essential for phosphate and vitamin D metabolism regulation. Its study using gene-knockout or conditional-knockout mouse models has provided insights into its role in diseases such as CKD, highlighting its significance in understanding bone-mineral metabolism-related pathologies.