scholarly journals The Roles of Specific Genes Implicated as Circulating Factors Involved in Normal and Disordered Phosphate Homeostasis: Frizzled Related Protein-4, Matrix Extracellular Phosphoglycoprotein, and Fibroblast Growth Factor 23

2006 ◽  
Vol 27 (3) ◽  
pp. 221-241 ◽  
Author(s):  
Kenneth E. White ◽  
Tobias E. Larsson ◽  
Michael J. Econs
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Related Protein ◽  
Phosphate Homeostasis ◽  
Matrix Extracellular Phosphoglycoprotein

Fibroblast growth factor 23 and calcium phosphate homeostasis after pediatric renal transplantation

2012 ◽  
Vol 16 (5) ◽  
pp. 443-450 ◽  
Author(s):  
Michael van Husen ◽  
Anja Lehnhardt ◽  
Ann-Katrin Fischer ◽  
Florian Brinkert ◽  
Sebastian Loos ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Growth Factor ◽  
Calcium Phosphate ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Pediatric Renal Transplantation ◽  
Phosphate Homeostasis

scholarly journals Oncogenic osteomalacia illustrating the effect of fibroblast growth factor 23 on phosphate homeostasis

2012 ◽  
Vol 5 (3) ◽  
pp. 240-243 ◽  
Author(s):  
P.-A. Westerberg ◽  
T. Linde ◽  
D. Vanderschueren ◽  
J. Billen ◽  
I. Jans ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Oncogenic Osteomalacia ◽  
Phosphate Homeostasis

scholarly journals Minireview: Fibroblast Growth Factor 23 in Phosphate Homeostasis and Bone Metabolism

Endocrinology ◽  
2011 ◽  
Vol 152 (1) ◽  
pp. 4-10 ◽  
Author(s):  
Michiko Hori ◽  
Yuichiro Shimizu ◽  
Seiji Fukumoto
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Bone Metabolism ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Phosphate Metabolism ◽  
Fibroblast Growth ◽  
Phosphate Homeostasis ◽  
Mineral And Bone Disorder ◽  
Bone Disorder

Abstract Fibroblast growth factor 23 (FGF23) was identified in 2000. Since then, FGF23 has been found to physiologically regulate phosphate metabolism and aberrant actions of FGF23 results in several disorders of phosphate and bone metabolism. In addition, FGF23 plays an important role in the development of chronic kidney disease–mineral and bone disorder. However, further investigations are necessary, especially with regard to the regulation of FGF23 expression. In this minireview, we focus on the physiological and pathophysiological significance of FGF23 in phosphate and bone metabolism.

scholarly journals The emerging role of the fibroblast growth factor-23–klotho axis in renal regulation of phosphate homeostasis

2007 ◽  
Vol 194 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Mohammed S Razzaque ◽  
Beate Lanske
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Ion Homeostasis ◽  
Experimental Studies ◽  
Receptor Activation ◽  
Fibroblast Growth ◽  
Phosphate Homeostasis ◽  
Downstream Signaling

Normal mineral ion homeostasis is tightly controlled by numerous endocrine factors that coordinately exert effects on intestine, kidney, and bone to maintain physiological balance. The importance of the fibroblast growth factor (FGF)-23–klotho axis in regulating mineral ion homeostasis has been proposed from recent research observations. Experimental studies suggest that 1) FGF23 is an important in vivo regulator of phosphate homeostasis, 2) FGF23 acts as a counter regulatory hormone to modulate the renal 1α-hydroxylase and sodium–phosphate cotransporter activities, 3) there is a trend of interrelationship between FGF23 and parathyroid hormone activities, 4) most of the FGF23 functions are conducted through the activation of FGF receptors, and 5) such receptor activation needs klotho, as a cofactor to generate downstream signaling events. These observations clearly suggest the emerging roles of the FGF23–klotho axis in maintaining mineral ion homeostasis. In this brief article, we will summarize how the FGF23–klotho axis might coordinately regulate normal mineral ion homeostasis, and how their abnormal regulation could severely disrupt such homeostasis to induce disease pathology.

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