The fibroblast growth factor 23: a new player in the field of cardiovascular, bone and renal disease.
Recently, a new view into the molecular mechanisms of phosphate homeostasis and secondary hyperparathyroidism pathogenesis has been proposed, with Fibroblast Growth Factor 23 (FGF-23) as a novel player in the field. Enhanced serum FGF-23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism. In contrast, reduced serum FGF-23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, there are different FGF-23 actions that need investigation. In clinical practice, increased knowledge of mineral metabolism disorders alterations in chronic kidney disease (CKD) may be used to improve diagnostics and select future treatments. The discovery of FGF23 represents a novel factor in the pathogenesis of phosphate handling and secondary hyperparathyroidism in cardiovascular, bone and renal disease.
Cozzolino
Mario
M
Renal Division, S. Paolo Hospital, University of Milan, 20142 Milan, Italy.
Mazzaferro
Sandro
S
D000818:Animals; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001847:Bone Diseases / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007674:Kidney Diseases / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D010710:Phosphates / Q000037:antagonists & inhibitors / Q000097:blood
D015415:Biomarkers; C000717427:FGF23 protein, human; D010710:Phosphates; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23