FGF23 (fibroblast growth factor 23) is a key endocrine regulator of phosphate and vitamin D metabolism. Its primary function involves controlling renal phosphate reabsorption by downregulating sodium-dependent phosphate transporters in proximal renal tubules 1. FGF23 signals through FGF receptors in conjunction with the co-receptor αKlotho, forming a critical regulatory axis for mineral metabolism 2. The protein suppresses 1α-hydroxylase expression, thereby reducing active vitamin D (calcitriol) production and maintaining phosphate homeostasis 1. Beyond its classical renal effects, FGF23 exhibits broader physiological roles including inhibition of bone mineralization and promotion of cardiac effects 3. Disease relevance is significant, as FGF23 overproduction causes hypophosphatemic rickets through excessive phosphate wasting 4. Elevated FGF23 levels are associated with cardiovascular complications, particularly left ventricular hypertrophy in chr12 kidney disease patients, where FGF23 can activate cardiac FGF receptors independently of αKlotho 5. Clinically, FGF23 serves both as a biomarker for mineral metabolism disorders and a potential therapeutic target, with anti-FGF23 antibody treatments under investigation for FGF23-dependent hypophosphatemic conditions 4 2.