Abstract
Fibroblast growth factor 23 (FGF23) plays an important role in the development of chronic kidney disease-mineral bone disorder (CKD-MBD). Abnormally elevated levels of 1,25-dihydroxyvitamin D cause osteocytes to secrete FGF23, which subsequently induces phosphaturia. Recent studies have reported that iron deficiency, erythropoietin (EPO) and hypoxia regulate the pathways responsible for FGF23 production. However, the molecular mechanisms underlying the interactions between FGF23 and anemia-related factors are not yet fully understood. The present review discusses the associations between FGF23, iron, EPO and hypoxia-inducible factors (HIFs), and their impact on FGF23 bioactivity, focusing on recent studies. Collectively, these findings propose interactions between FGF23 gene expression and anemia-related factors, including iron deficiency, EPO and HIFs. Taken together, these results suggest that FGF23 bioactivity is closely associated with the occurrence of CKD-related anemia and CKD-MBD.