Abstract
Fibroblast growth factor (FGF)-23 is a bone-derived hormone that is mainly binded to FGF receptor/Klotho combination. Numerous factors have been implicated in the physiological and pathological regulation of FGF-23 expression. FGF-23 has been originally shown to function as a central regulator of phosphate and vitamin D metabolism. Disruption of FGF-23 in metabolic homeostasis plays a significant role in the pathogenesis of phosphate-associated diseases, including X-link dominate hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, autosomal recessive hypophosphatemic rickets and tumor-induced osteomalacia. Accompanied with further studies, high level of FGF-23 is pathologically involved in the development of chronic kidney disease and cardiovascular disease. The precise metabolic regulation and molecular mechanisms of FGF-23 underlying these conditions remain to be elucidated. Moreover, the emerging roles of FGF-23 in glucose and lipid metabolism have been investigated. Key words: Fibroblast growth factor-23; Klotho; Phosphate homeostasis; Chronic kidney disease; Cardiovascular disease
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