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Gene Review

Fgf23  -  fibroblast growth factor 23

Mus musculus

Synonyms: FGF-23, Fibroblast growth factor 23
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Disease relevance of Fgf23


High impact information on Fgf23

  • Both Dmp1-null mice and individuals with a newly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting associated with elevated fibroblast growth factor 23 (FGF23) levels and normocalciuria [5].
  • Vitamin D receptor in chondrocytes promotes osteoclastogenesis and regulates FGF23 production in osteoblasts [6].
  • Disruption of the Fgf23 gene did not result in embryonic lethality, although homozygous mice showed severe growth retardation with abnormal bone phenotype and markedly short life span [7].
  • These phenotypes could not be explained by currently known regulators of mineral homeostasis, indicating that FGF23 is essential for normal phosphate and vitamin D metabolism [7].
  • We present here the evidence that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF23-null mice [7].

Chemical compound and disease context of Fgf23


Biological context of Fgf23


Anatomical context of Fgf23

  • Surprisingly, eGFP expression was not increased in cell surface osteoblasts, indicating that Phex deficiency is necessary but not sufficient for increased Fgf23 expression in the osteoblast lineage [1].
  • Additional factors, associated with either osteocyte differentiation and/or extracellular matrix, are necessary for Phex deficiency to stimulate Fgf23 gene transcription in bone [1].
  • Because mouse Fgf23 mRNA was expressed in dendritic cells and activated spleen, tumor infiltrating dendritic cells are candidate sources of FGF23 secretion in TIO patients [14].
  • Therefore, we examined the mechanism of action of FGF-23 in cultured renal proximal epithelial cells, opossum kidney cells [15].
  • Fgf-23 mRNA abundance in calvaria was significantly higher in Hyp mice than in WT mice on the 1% Pi diet; in both groups of mice, fgf-23 mRNA abundance in calvarial bone was suppressed by 85% on the low (0.02%) Pi diet [12].

Associations of Fgf23 with chemical compounds


Physical interactions of Fgf23

  • FGF-23 binds to the FGF receptor 3c, which is mainly expressed in opossum kidney cells, with high affinity [15].

Regulatory relationships of Fgf23

  • CONCLUSIONS: FGF-23 regulates NaPi-2a independently of PTH and the serum 1,25(OH)2D level by controlling renal expressions of key enzymes of the vitamin D metabolism [17].

Other interactions of Fgf23

  • The authors found that Hyp mice had increased expression of the MEPE and another phosphaturic factor, Fgf23 [18].
  • Normalization of serum phosphate by diet in VDR(-/-) mice increases Fgf23 [2].
  • In Npt2a(-/-) mice, serum FGF-23 concentrations were significantly lower than in WT mice, and these differences could be accounted for by the lower serum Pi levels in Npt2a(-/-) mice [12].
  • Finally, our data support a new model of interactions among Fgf-23, vitamin D, and klotho, a gene described as being associated with premature aging process [19].
  • FGF-23 reduced renal mRNA for 25-hydroxyvitamin D-1alpha-hydroxylase and increased that for 25-hydroxyvitamin D-24-hydroxylase starting at 1 h [17].

Analytical, diagnostic and therapeutic context of Fgf23

  • Genetic dissection of phosphate- and vitamin D-mediated regulation of circulating Fgf23 concentrations [2].
  • In contrast, by real-time reverse transcriptase PCR, the levels of fgf23 transcripts were highest in bone, the predominant site of Phex expression [20].
  • In osteoblast cell cultures, 1,25(OH)(2)D(3) but not calcium, phosphate, or parathyroid hormone stimulated FGF23 mRNA levels and resulted in a dose-dependent increase in FGF23 promoter activity [21].
  • The localization of FGF-23 mRNA in the brain was examined by in situ hybridization [22].
  • Western blot analysis using site-specific antibodies showed that wild-type FGF-23 secreted into conditioned media was partially cleaved between Arg(179) and Ser(180) [23].


  1. Pathogenic role of Fgf23 in Hyp mice. Liu, S., Zhou, J., Tang, W., Jiang, X., Rowe, D.W., Quarles, L.D. Am. J. Physiol. Endocrinol. Metab. (2006) [Pubmed]
  2. Genetic dissection of phosphate- and vitamin D-mediated regulation of circulating Fgf23 concentrations. Yu, X., Sabbagh, Y., Davis, S.I., Demay, M.B., White, K.E. Bone (2005) [Pubmed]
  3. Fibroblast growth factor-23 increases mouse PGE2 production in vivo and in vitro. Syal, A., Schiavi, S., Chakravarty, S., Dwarakanath, V., Quigley, R., Baum, M. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  4. A novel recessive mutation in fibroblast growth factor-23 causes familial tumoral calcinosis. Larsson, T., Yu, X., Davis, S.I., Draman, M.S., Mooney, S.D., Cullen, M.J., White, K.E. J. Clin. Endocrinol. Metab. (2005) [Pubmed]
  5. Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. Feng, J.Q., Ward, L.M., Liu, S., Lu, Y., Xie, Y., Yuan, B., Yu, X., Rauch, F., Davis, S.I., Zhang, S., Rios, H., Drezner, M.K., Quarles, L.D., Bonewald, L.F., White, K.E. Nat. Genet. (2006) [Pubmed]
  6. Vitamin D receptor in chondrocytes promotes osteoclastogenesis and regulates FGF23 production in osteoblasts. Masuyama, R., Stockmans, I., Torrekens, S., Van Looveren, R., Maes, C., Carmeliet, P., Bouillon, R., Carmeliet, G. J. Clin. Invest. (2006) [Pubmed]
  7. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. Shimada, T., Kakitani, M., Yamazaki, Y., Hasegawa, H., Takeuchi, Y., Fujita, T., Fukumoto, S., Tomizuka, K., Yamashita, T. J. Clin. Invest. (2004) [Pubmed]
  8. FGF-23 transgenic mice demonstrate hypophosphatemic rickets with reduced expression of sodium phosphate cotransporter type IIa. Shimada, T., Urakawa, I., Yamazaki, Y., Hasegawa, H., Hino, R., Yoneya, T., Takeuchi, Y., Fujita, T., Fukumoto, S., Yamashita, T. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  9. The phosphatonins and the regulation of phosphate transport and vitamin D metabolism. Sommer, S., Berndt, T., Craig, T., Kumar, R. J. Steroid Biochem. Mol. Biol. (2007) [Pubmed]
  10. Sodium-phosphate cotransporters, nephrolithiasis and bone demineralization. Prié, D., Beck, L., Friedlander, G., Silve, C. Curr. Opin. Nephrol. Hypertens. (2004) [Pubmed]
  11. Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice. Sitara, D., Razzaque, M.S., Hesse, M., Yoganathan, S., Taguchi, T., Erben, R.G., Jüppner, H., Lanske, B. Matrix Biol. (2004) [Pubmed]
  12. Dietary and serum phosphorus regulate fibroblast growth factor 23 expression and 1,25-dihydroxyvitamin D metabolism in mice. Perwad, F., Azam, N., Zhang, M.Y., Yamashita, T., Tenenhouse, H.S., Portale, A.A. Endocrinology (2005) [Pubmed]
  13. Vitamin D and phosphate regulate fibroblast growth factor-23 in K-562 cells. Ito, M., Sakai, Y., Furumoto, M., Segawa, H., Haito, S., Yamanaka, S., Nakamura, R., Kuwahata, M., Miyamoto, K. Am. J. Physiol. Endocrinol. Metab. (2005) [Pubmed]
  14. Comparative genomics on mammalian Fgf6-Fgf23 locus. Katoh, Y., Katoh, M. Int. J. Mol. Med. (2005) [Pubmed]
  15. Fibroblast growth factor (FGF)-23 inhibits renal phosphate reabsorption by activation of the mitogen-activated protein kinase pathway. Yamashita, T., Konishi, M., Miyake, A., Inui, K., Itoh, N. J. Biol. Chem. (2002) [Pubmed]
  16. Role of the vitamin D receptor in FGF23 action on phosphate metabolism. Inoue, Y., Segawa, H., Kaneko, I., Yamanaka, S., Kusano, K., Kawakami, E., Furutani, J., Ito, M., Kuwahata, M., Saito, H., Fukushima, N., Kato, S., Kanayama, H.O., Miyamoto, K. Biochem. J. (2005) [Pubmed]
  17. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. Shimada, T., Hasegawa, H., Yamazaki, Y., Muto, T., Hino, R., Takeuchi, Y., Fujita, T., Nakahara, K., Fukumoto, S., Yamashita, T. J. Bone Miner. Res. (2004) [Pubmed]
  18. Role of matrix extracellular phosphoglycoprotein in the pathogenesis of X-linked hypophosphatemia. Liu, S., Brown, T.A., Zhou, J., Xiao, Z.S., Awad, H., Guilak, F., Quarles, L.D. J. Am. Soc. Nephrol. (2005) [Pubmed]
  19. Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process. Razzaque, M.S., Sitara, D., Taguchi, T., St-Arnaud, R., Lanske, B. FASEB J. (2006) [Pubmed]
  20. Regulation of fibroblastic growth factor 23 expression but not degradation by PHEX. Liu, S., Guo, R., Simpson, L.G., Xiao, Z.S., Burnham, C.E., Quarles, L.D. J. Biol. Chem. (2003) [Pubmed]
  21. Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin d. Liu, S., Tang, W., Zhou, J., Stubbs, J.R., Luo, Q., Pi, M., Quarles, L.D. J. Am. Soc. Nephrol. (2006) [Pubmed]
  22. Identification of a novel fibroblast growth factor, FGF-23, preferentially expressed in the ventrolateral thalamic nucleus of the brain. Yamashita, T., Yoshioka, M., Itoh, N. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  23. Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Shimada, T., Muto, T., Urakawa, I., Yoneya, T., Yamazaki, Y., Okawa, K., Takeuchi, Y., Fujita, T., Fukumoto, S., Yamashita, T. Endocrinology (2002) [Pubmed]
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