Skip to main content
SpringerLink
Log in

FGF23 as a Novel Therapeutic Target

  • Chapter
Endocrine FGFs and Klothos

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 728))

Abstract

Fibroblast growth factor (FGF) 23 is a hormone that acts to decrease phosphate, 1,25-dihydroxyvitamin D and parathyroid hormone levels in circulation. Particularly, appropriate actions of FGF23 are essential for maintaining physiological phosphate and vitamin D metabolism. Therefore, either gain or loss of function of FGF23 can impair these homeostatic regulations, causing several metabolic bone diseases. The measurement of circulating levels of FGF23 in patients with various types of hypophosphatemic rickets and/or osteomalacia has revealed that several of them are FGF23-dependent diseases, highlighting a novel therapeutic concept that the inhibition of the excess activity of FGF23 could be beneficial for patients with these diseases. Indeed, preliminary studies with a mouse disease model have validated this concept. On the other hand, replacement therapy with recombinant FGF23 may be applied to the disease caused by loss of function of FGF23. Although these concepts still need to be proven with more detailed analyses, the latest knowledge on the FGF23-related diseases and the development of methods to appropriately regulate FGF23 actions may synergistically create novel therapeutic maneuvers.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 129.00
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Yamashita T, Yoshioka M, Itoh N. Identification of a novel fibroblast growth factor, FGF-23, preferentially expressed in the ventrolateral thalamic nucleus of the brain. Biochem Biophys Res Commun 2000; 277:494–498.

    Article  PubMed  CAS  Google Scholar 

  2. The ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet 2000; 26:345–348.

    Google Scholar 

  3. White KE, Jonsson KB, Carn G et al. The autosomal dominant hypophosphatemic rickets (ADHR) gene is a secreted polypeptide overexpressed by tumors that cause phosphate wasting. J Clin Endocrinol Metab 2001; 86:497–500.

    Article  PubMed  CAS  Google Scholar 

  4. Shimada T, Mizutani S, Muto T et al. Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proc Natl Acad Sci USA 2001; 98:6500–6505.

    Article  PubMed  CAS  Google Scholar 

  5. Shimada T, Muto T, Urakawa I et al. Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Endocrinology 2002; 143:3179–3182.

    Article  PubMed  CAS  Google Scholar 

  6. Bai XY, Miao D, Goltzman D et al. The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency. J Biol Chem 2003; 278:9843–9849.

    Article  PubMed  CAS  Google Scholar 

  7. Bai X, Miao D, Li J et al. Transgenic mice overexpressing human fibroblast growth factor 23 (R176Q) delineate a putative role for parathyroid hormone in renal phosphate wasting disorders. Endocrinology 2004; 145:5269–5279.

    Article  PubMed  CAS  Google Scholar 

  8. Larsson T, Marsell R, Schipani E et al. Transgenic mice expressing fibroblast growth factor 23 under the control of the alpha1(I) collagen promoter exhibit growth retardation, osteomalacia and disturbed phosphate homeostasis. Endocrinology 2004; 145:3087–3094.

    Article  PubMed  CAS  Google Scholar 

  9. Shimada T, Urakawa I, Yamazaki Y et al. FGF-23 transgenic mice demonstrate hypophosphatemic rickets with reduced expression of sodium phosphate cotransporter type IIa. Biochem Biophys Res Commun 2004; 314:409–414.

    Article  PubMed  CAS  Google Scholar 

  10. Yamamoto T, Imanishi Y, Kinoshita E et al. The role of fibroblast growth factor 23 for hypophosphatemia and abnormal regulation of vitamin D metabolism in patients with McCune-Albright syndrome. J Bone Miner Metab 2005; 23:231–237.

    Article  PubMed  CAS  Google Scholar 

  11. Weber TJ, Liu S, Indridason OS et al. Serum FGF23 levels in normal and disordered phosphorus homeostasis. J Bone Miner Res 2003; 18:1227–1234.

    Article  PubMed  CAS  Google Scholar 

  12. Riminucci M, Collins MT, Fedarko NS et al. FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting. J Clin Invest 2003; 112:683–692.

    PubMed  CAS  Google Scholar 

  13. Jonsson KB, Zahradnik R, Larsson T et al. Fibroblast growth factor 23 in oncogenic osteomalacia and X-linked hypophosphatemia. N Engl J Med 2003; 348:1656–1663.

    Article  PubMed  CAS  Google Scholar 

  14. Yamazaki Y, Okazaki R, Shibata M et al. Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia. J Clin Endocrinol Metab 2002; 87:4957–4960.

    Article  PubMed  CAS  Google Scholar 

  15. Endo I, Fukumoto S, Ozono K et al. Clinical usefulness of measurement of fibroblast growth factor 23 (FGF23) in hypophosphatemic patients: proposal of diagnostic criteria using FGF23 measurement. Bone 2008; 42:1235–1239.

    Article  PubMed  CAS  Google Scholar 

  16. Burnett SM, Gunawardene SC, Bringhurst FR et al. Regulation of C-terminal and intact FGF-23 by dietary phosphate in men and women. J Bone Miner Res 2006; 21:1187–1196.

    Article  PubMed  CAS  Google Scholar 

  17. Ferrari SL, Bonjour JP, Rizzoli R. Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. J Clin Endocrinol Metab 2005; 90:1519–1524.

    Article  PubMed  CAS  Google Scholar 

  18. Shimada T, Kakitani M, Yamazaki Y et al. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. J Clin Invest 2004; 113:561–568.

    PubMed  CAS  Google Scholar 

  19. Sitara D, Razzaque MS, Hesse M et al. Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis and reverses hypophosphatemia in Phex-deficient mice. Matrix Biol 2004; 23:421–432.

    Article  PubMed  CAS  Google Scholar 

  20. Lyles KW, Burkes EJ, Ellis GJ et al. Genetic transmission of tumoral calcinosis: autosomal dominant with variable clinical expressivity. J Clin Endocrinol Metab 1985; 60:1093–1096.

    Article  PubMed  CAS  Google Scholar 

  21. Slavin RE, Wen J, Kumar D et al. Familial tumoral calcinosis. A clinical, histopathologic and ultrastructural study with an analysis of its calcifying process and pathogenesis. Am J Surg Pathol 1993; 17:788–802.

    Article  PubMed  CAS  Google Scholar 

  22. Topaz O, Shurman DL, Bergman R et al. Mutations in GALNT3, encoding a protein involved in O-linked glycosylation, cause familial tumoral calcinosis. Nat Genet 2004; 36:579–581.

    Article  PubMed  CAS  Google Scholar 

  23. Araya K, Fukumoto S, Backenroth R et al. A novel mutation in fibroblast growth factor 23 gene as a cause of tumoral calcinosis. J Clin Endocrinol Metab 2005; 90:5523–5527.

    Article  PubMed  CAS  Google Scholar 

  24. Benet-Pages A, Orlik P, Strom TM et al. An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia. Hum Mol Genet 2005; 14:385–390.

    Article  PubMed  CAS  Google Scholar 

  25. Chefetz I, Heller R, Galli-Tsinopoulou A et al. A novel homozygous missense mutation in FGF23 causes Familial Tumoral Calcinosis associated with disseminated visceral calcification. Hum Genet 2005; 118:261–266.

    Article  PubMed  CAS  Google Scholar 

  26. Larsson T, Davis SI, Garringer HJ et al. Fibroblast growth factor-23 mutants causing familial tumoral calcinosis are differentially processed. Endocrinology 2005; 146:3883–3891.

    Article  PubMed  CAS  Google Scholar 

  27. Larsson T, Yu X, Davis SI et al. A novel recessive mutation in fibroblast growth factor-23 causes familial tumoral calcinosis. J Clin Endocrinol Metab 2005; 90:2424–2427.

    Article  PubMed  CAS  Google Scholar 

  28. Ben-Dov IZ, Galitzer H, Lavi-Moshayoff V et al. The parathyroid is a target organ for FGF23 in rats. J Clin Invest 2007; 117:4003–4008.

    PubMed  CAS  Google Scholar 

  29. Krajisnik T, Bjorklund P, Marsell R et al. Fibroblast growth factor-23 regulates parathyroid hormone and 1alpha-hydroxylase expression in cultured bovine parathyroid cells. J Endocrinol 2007; 195:125–131.

    Article  PubMed  CAS  Google Scholar 

  30. Saito H, Kusano K, Kinosaki M et al. Human fibroblast growth factor-23 mutants suppress Na+-dependent phosphate cotransport activity and 1alpha, 25-dihydroxyvitamin D3 production. J Biol Chem 2003; 278:2206–2211.

    Article  PubMed  CAS  Google Scholar 

  31. Shimada T, Hasegawa H, Yamazaki Y et al. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. J Bone Miner Res 2004; 19:429–435.

    Article  PubMed  CAS  Google Scholar 

  32. Bikle D, Adams J, Christakos S. Vitamin D: Production, metabolism, mechanism of action and clinical requirements. In: Seeman E, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th ed. Washington D.C.: The American Society for Bone and Research, 2008; 141–149.

    Chapter  Google Scholar 

  33. Favus M, Bushinsky DA, Lemann J. Regulation of calcium, magnesium and phosphate metabolism. In: Christakos S, Holick MF, eds. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, sixth ed. Washington, D.C.: the American Society for Bone and Mineral Research, 2006; 76–83.

    Google Scholar 

  34. Miyamoto K, Ito M, Tatsumi S et al. New aspect of renal phosphate reabsorption: the type IIc sodium-dependent phosphate transporter. Am J Nephrol 2007; 27:503–515.

    Article  PubMed  CAS  Google Scholar 

  35. Tenenhouse HS. Phosphate transport: molecular basis, regulation and pathophysiology. J Steroid Biochem Mol Biol 2007; 103:572–577.

    Article  PubMed  CAS  Google Scholar 

  36. Beck L, Karaplis AC, Amizuka N et al. Targeted inactivation of Npt2 in mice leads to severe renal phosphate wasting, hypercalciuria and skeletal abnormalities. Proc Natl Acad Sci USA 1998; 95:5372–5377.

    Article  PubMed  CAS  Google Scholar 

  37. Segawa H, Onitsuka A, Furutani J et al. Npt2a and Npt2c in mice play distinct and synergistic roles in inorganic phosphate metabolism and skeletal development. Am J Physiol Renal Physiol 2009; 297:F671–678.

    Article  PubMed  CAS  Google Scholar 

  38. Bergwitz C, Roslin NM, Tieder M et al. SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis. Am J Hum Genet 2006; 78:179–192.

    Article  PubMed  CAS  Google Scholar 

  39. Ichikawa S, Sorenson AH, Imel EA et al. Intronic deletions in the SLC34A3 gene cause hereditary hypophosphatemic rickets with hypercalciuria. J Clin Endocrinol Metab 2006; 91:4022–4027.

    Article  PubMed  CAS  Google Scholar 

  40. Lorenz-Depiereux B, Benet-Pages A, Eckstein G et al. Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. Am J Hum Genet 2006; 78:193–201.

    Article  PubMed  CAS  Google Scholar 

  41. Yamamoto T, Michigami T, Aranami F et al. Hereditary hypophosphatemic rickets with hypercalciuria: a study for the phosphate transporter gene type IIc and osteoblastic function. J Bone Miner Metab 2007; 25:407–413.

    Article  PubMed  Google Scholar 

  42. Bastepe M, Juppner H. Inherited hypophosphatemic disorders in children and the evolving mechanisms of phosphate regulation. Rev Endocr Metab Disord 2008; 9:171–180.

    Article  PubMed  Google Scholar 

  43. Jaureguiberry G, Carpenter TO, Forman S et al. A novel missense mutation in SLC34A3 that causes hereditary hypophosphatemic rickets with hypercalciuria in humans identifies threonine 137 as an important determinant of sodium-phosphate cotransport in NaPi-IIc. Am J Physiol Renal Physiol 2008; 295:F371–379.

    Article  PubMed  CAS  Google Scholar 

  44. Levi M. Novel NaPi-2c mutations that cause mistargeting of NaPi-2c protein and uncoupling of Na-Pi cotransport cause HHRH. Am J Physiol Renal Physiol 2008; 295:F369–370.

    Article  PubMed  CAS  Google Scholar 

  45. Yamashita T, Konishi M, Miyake A et al. Fibroblast growth factor (FGF)-23 inhibits renal phosphate reabsorption by activation of the mitogen-activated protein kinase pathway. J Biol Chem 2002; 277:28265–28270.

    Article  PubMed  CAS  Google Scholar 

  46. Segawa H, Kawakami E, Kaneko I et al. Effect of hydrolysis-resistant FGF23-R179Q on dietary phosphate regulation of the renal type-II Na/Pi transporter. Pflugers Arch 2003; 446:585–592.

    Article  PubMed  CAS  Google Scholar 

  47. Baum M, Schiavi S, Dwarakanath V et al. Effect of fibroblast growth factor-23 on phosphate transport in proximal tubules. Kidney Int 2005; 68:1148–1153.

    Article  PubMed  CAS  Google Scholar 

  48. Pfister MF, Ruf I, Stange G et al. Parathyroid hormone leads to the lysosomal degradation of the renal type II Na/Pi cotransporter. Proc Natl Acad Sci USA 1998; 95:1909–1914.

    Article  PubMed  CAS  Google Scholar 

  49. Yamamoto H, Tani Y, Kobayashi K et al. Alternative promoters and renal cell-specific regulation of the mouse type IIa sodium-dependent phosphate cotransporter gene. Biochim Biophys Acta 2005; 1732:43–52.

    PubMed  CAS  Google Scholar 

  50. Inoue Y, Segawa H, Kaneko I et al. Role of the vitamin D receptor in FGF23 action on phosphate metabolism. Biochem J 2005; 390:325–331.

    Article  PubMed  CAS  Google Scholar 

  51. Shimada T, Yamazaki Y, Takahashi M et al. Vitamin D receptor-independent FGF23 actions in regulating phosphate and vitamin D metabolism. Am J Physiol Renal Physiol 2005; 289:F1088–1095.

    Article  PubMed  CAS  Google Scholar 

  52. Fukagawa M, Nii-Kono T, Kazama JJ. Role of fibroblast growth factor 23 in health and in chronic kidney disease. Curr Opin Nephrol Hypertens 2005; 14:325–329.

    Article  PubMed  CAS  Google Scholar 

  53. Gutierrez O, Isakova T, Rhee E et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am Soc Nephrol 2005; 16:2205–2215.

    Article  PubMed  CAS  Google Scholar 

  54. Kazama JJ, Gejyo F, Shigematsu T et al. Role of circulating fibroblast growth factor 23 in the development of secondary hyperparathyroidism. Ther Apher Dial 2005; 9:328–330.

    Article  PubMed  CAS  Google Scholar 

  55. Drezner MK, Feinglos MN. Osteomalacia due to 1alpha,25-dihydroxycholecalciferol deficiency. Association with a giant cell tumor of bone. J Clin Invest 1977; 60:1046–1053.

    Article  PubMed  CAS  Google Scholar 

  56. Econs MJ, Drezner MK. Tumor-induced osteomalacia—unveiling a new hormone. N Engl J Med 1994; 330:1679–1681.

    Article  PubMed  CAS  Google Scholar 

  57. Goetz R, Beenken A, Ibrahimi OA et al. Molecular insights into the klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members. Mol Cell Biol 2007; 27:3417–3428.

    Article  PubMed  CAS  Google Scholar 

  58. Beenken A, Mohammadi M. The FGF family: biology, pathophysiology and therapy. Nat Rev Drug Discov 2009; 8:235–253.

    Article  PubMed  CAS  Google Scholar 

  59. Kurosu H, Ogawa Y, Miyoshi M et al. Regulation of fibroblast growth factor-23 signaling by klotho. J Biol Chem 2006; 281:6120–6123.

    Article  PubMed  CAS  Google Scholar 

  60. Urakawa I, Yamazaki Y, Shimada T et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature 2006; 444:770–774.

    Article  PubMed  CAS  Google Scholar 

  61. Kuroo M, Matsumura Y, Aizawa H et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature 1997; 390:45–51.

    Article  CAS  Google Scholar 

  62. Yu X, Ibrahimi OA, Goetz R et al. Analysis of the biochemical mechanisms for the endocrine actions of fibroblast growth factor-23. Endocrinology 2005; 146:4647–4656.

    Article  PubMed  CAS  Google Scholar 

  63. Mirams M, Robinson BG, Mason RS et al. Bone as a source of FGF23: regulation by phosphate? Bone 2004; 35:1192–1199.

    Article  PubMed  CAS  Google Scholar 

  64. Liu S, Zhou J, Tang W et al. Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab 2006; 291:E38–49.

    Article  PubMed  CAS  Google Scholar 

  65. Yamazaki Y, Tamada T, Kasai N et al. Anti-FGF23 neutralizing antibodies show the physiological role and structural features of FGF23. J Bone Miner Res 2008; 23:1509–1518.

    Article  PubMed  CAS  Google Scholar 

  66. Liu S, Vierthaler L, Tang W et al. FGFR3 and FGFR4 do not mediate renal effects of FGF23. J Am Soc Nephrol 2008; 19:2342–2350.

    Article  PubMed  CAS  Google Scholar 

  67. Gattineni J, Bates C, Twombley K et al. FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Renal Physiol 2009; 297:F282–291.

    Article  PubMed  CAS  Google Scholar 

  68. Segawa H, Yamanaka S, Ohno Y et al. Correlation between hyperphosphatemia and type II Na-Pi cotransporter activity in klotho mice. Am J Physiol Renal Physiol 2007; 292:F769–779.

    Article  PubMed  CAS  Google Scholar 

  69. Ichikawa S, Imel EA, Kreiter ML et al. A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis. J Musculoskelet Neuronal Interact 2007; 7:318–319.

    PubMed  CAS  Google Scholar 

  70. Drezner MK. PHEX gene and hypophosphatemia. Kidney Int 2000; 57:9–18.

    Article  PubMed  CAS  Google Scholar 

  71. The HYP Consortium. A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. Nat Genet 1995; 11:130–136.

    Google Scholar 

  72. Beck L, Soumounou Y, Martel J et al. Pex/PEX tissue distribution and evidence for a deletion in the 3′ region of the Pex gene in X-linked hypophosphatemic mice. J Clin Invest 1997; 99:1200–1209.

    Article  PubMed  CAS  Google Scholar 

  73. Meyer RA Jr, Meyer MH, Gray RW. Parabiosis suggests a humoral factor is involved in X-linked hypophosphatemia in mice. J Bone Miner Res 1989; 4:493–500.

    Article  PubMed  Google Scholar 

  74. Meyer RA Jr, Tenenhouse HS, Meyer MH et al. The renal phosphate transport defect in normal mice parabiosed to X-linked hypophosphatemic mice persists after parathyroidectomy. J Bone Miner Res 1989; 4:523–532.

    Article  PubMed  CAS  Google Scholar 

  75. Nesbitt T, Coffman TM, Griffiths R et al. Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect. J Clin Invest 1992; 89:1453–1459.

    Article  PubMed  CAS  Google Scholar 

  76. Grieff M. New insights into X-linked hypophosphatemia. Curr Opin Nephrol Hypertens 1997; 6:15–19.

    Article  PubMed  CAS  Google Scholar 

  77. Nelson AE, Mason RS, Robinson BG. The PEX gene: not a simple answer for X-linked hypophosphataemic rickets and oncogenic osteomalacia. Mol Cell Endocrinol 1997; 132:1–5.

    Article  PubMed  CAS  Google Scholar 

  78. Aono Y, Yamazaki Y, Yasutake J et al. Therapeutic Effects of Anti-FGF23 Antibodies in Hypophosphatemic Rickets/Osteomalacia. J Bone Miner Res 2009; 24:1879–1888.

    Article  PubMed  CAS  Google Scholar 

  79. Kang Y, Zhang R, Lu Y et al. Crossing Talk between Pi homeostasis and Bone. J Bone Miner Res 2009; 24.

    Google Scholar 

  80. Feng JQ, Ward LM, Liu S et al. Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. Nat Genet 2006; 38:1310–1315.

    Article  PubMed  CAS  Google Scholar 

  81. Lorenz-Depiereux B, Bastepe M, Benet-Pages A et al. DMP1 mutations in autosomal recessive hypophosphatemia implicate a bone matrix protein in the regulation of phosphate homeostasis. Nat Genet 2006; 38:1248–1250.

    Article  PubMed  CAS  Google Scholar 

  82. Fukumoto S. Physiological regulation and disorders of phosphate metabolism—pivotal role of fibroblast growth factor 23. Intern Med 2008; 47:337–343.

    Article  PubMed  Google Scholar 

  83. Frishberg Y, Ito N, Rinat C et al. Hyperostosis-hyperphosphatemia syndrome: a congenital disorder of O-glycosylation associated with augmented processing of fibroblast growth factor 23. J Bone Miner Res 2007; 22:235–242.

    Article  PubMed  CAS  Google Scholar 

  84. Ichikawa S, Sorenson AH, Austin AM et al. Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression. Endocrinology 2009; 150:254

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Innovative Drug Research Laboratories, Kyowa Hakko Kirin Co., Ltd, Tokyo, Japan

    Takashi Shimada

  2. Japan Division of Nephrology and Endocrinology Department of Medicine, University of Tokyo Hospital, Tokyo, Japan

    Seiji Fukumoto

Authors
  1. Takashi Shimada
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Seiji Fukumoto
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Takashi Shimada .

Editor information

Editors and Affiliations

  1. Department of Pathology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA

    Makoto Kuro-o MD, PhD

Rights and permissions

Reprints and permissions

Copyright information

© 2012 Landes Bioscience and Springer Science+Business Media

About this chapter

Cite this chapter

Shimada, T., Fukumoto, S. (2012). FGF23 as a Novel Therapeutic Target. In: Kuro-o, M. (eds) Endocrine FGFs and Klothos. Advances in Experimental Medicine and Biology, vol 728. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-0887-1_10

Download citation

Publish with us

Policies and ethics

Search

Navigation