Skip to main content
Erschienen in: Pediatric Nephrology 4/2013

01.04.2013 | Review

FGF23 production by osteocytes

verfasst von: Lynda F. Bonewald, Michael J. Wacker

Erschienen in: Pediatric Nephrology | Ausgabe 4/2013

Einloggen, um Zugang zu erhalten

Abstract

Fibroblast Growth Factor 23 (FGF23), a known regulator of phosphate homeostasis, is produced by cells residing in bone, namely, osteocytes, to target a distant organ, the kidney. Elevated FGF23 levels have recently been found systemically and in osteocytes in patients and animal models of chronic kidney disease. Associations between serum FGF23 level and vascular dysfunction, vascular calcification, and increased risk of cardiovascular disease have also been observed. In this review we discuss FGF23 expression in osteocytes and the potential means to regulate expression and function of this protein at the osteocyte level.
Literatur
1.
Zurück zum Zitat Parfitt AM (1977) The cellular basis of bone turnover and bone loss: A rebuttal of the osteocytic resorption–bone flow theory. Clin Orthop Relat Res 127:236–247PubMed Parfitt AM (1977) The cellular basis of bone turnover and bone loss: A rebuttal of the osteocytic resorption–bone flow theory. Clin Orthop Relat Res 127:236–247PubMed
2.
Zurück zum Zitat Kamioka H, Honjo T, Takano-Yamamoto T (2001) A three-dimensional distribution of osteocyte processes revealed by the combination of confocal laser scanning microscopy and differential interference contrast microscopy. Bone 28:145–149PubMedCrossRef Kamioka H, Honjo T, Takano-Yamamoto T (2001) A three-dimensional distribution of osteocyte processes revealed by the combination of confocal laser scanning microscopy and differential interference contrast microscopy. Bone 28:145–149PubMedCrossRef
3.
Zurück zum Zitat Lanyon LE (1993) Osteocytes, strain detection, bone modeling and remodeling. Calcif Tissue Int 53:S102–S106, discussion S106-107PubMedCrossRef Lanyon LE (1993) Osteocytes, strain detection, bone modeling and remodeling. Calcif Tissue Int 53:S102–S106, discussion S106-107PubMedCrossRef
5.
Zurück zum Zitat Yamashita T, Yoshioka M, Itoh N (2000) Identification of a novel fibroblast growth factor, FGF-23, preferentially expressed in the ventrolateral thalamic nucleus of the brain. Biochem Biophys Res Commun 277:494–498PubMedCrossRef Yamashita T, Yoshioka M, Itoh N (2000) Identification of a novel fibroblast growth factor, FGF-23, preferentially expressed in the ventrolateral thalamic nucleus of the brain. Biochem Biophys Res Commun 277:494–498PubMedCrossRef
6.
Zurück zum Zitat Shimada T, Kakitani M, Yamazaki Y, Hasegawa H, Takeuchi Y, Fujita T, Fukumoto S, Tomizuka K, Yamashita T (2004) Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. J Clin Invest 113:561–568PubMed Shimada T, Kakitani M, Yamazaki Y, Hasegawa H, Takeuchi Y, Fujita T, Fukumoto S, Tomizuka K, Yamashita T (2004) Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. J Clin Invest 113:561–568PubMed
7.
Zurück zum Zitat Feng JQ, Ward LM, Liu S, Lu Y, Xie Y, Yuan B, Yu X, Rauch F, Davis SI, Zhang S, Rios H, Drezner MK, Quarles LD, Bonewald LF, White KE (2006) Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. Nat Genet 38:1310–1315PubMedCrossRef Feng JQ, Ward LM, Liu S, Lu Y, Xie Y, Yuan B, Yu X, Rauch F, Davis SI, Zhang S, Rios H, Drezner MK, Quarles LD, Bonewald LF, White KE (2006) Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. Nat Genet 38:1310–1315PubMedCrossRef
8.
Zurück zum Zitat Liu S, Bo Y, Xie Y, Zhou J, Quarles LD, Bonewald L, Feng JQ (2006) Elevated levels of FGF23 in Dentin Matrix Protein 1 (DMP1) Null Mice Potentially Explain Phenotypic Similarities to Hyp Mice. J BoneMin Res 21[Suppl 1]:S51 Liu S, Bo Y, Xie Y, Zhou J, Quarles LD, Bonewald L, Feng JQ (2006) Elevated levels of FGF23 in Dentin Matrix Protein 1 (DMP1) Null Mice Potentially Explain Phenotypic Similarities to Hyp Mice. J BoneMin Res 21[Suppl 1]:S51
9.
Zurück zum Zitat Liu S, Rowe PS, Vierthaler L, Zhou J, Quarles LD (2007) Phosphorylated acidic serine–aspartate-rich MEPE-associated motif peptide from matrix extracellular phosphoglycoprotein inhibits phosphate regulating gene with homologies to endopeptidases on the X-chromosome enzyme activity. J Endocrinol 192:261–267PubMedCrossRef Liu S, Rowe PS, Vierthaler L, Zhou J, Quarles LD (2007) Phosphorylated acidic serine–aspartate-rich MEPE-associated motif peptide from matrix extracellular phosphoglycoprotein inhibits phosphate regulating gene with homologies to endopeptidases on the X-chromosome enzyme activity. J Endocrinol 192:261–267PubMedCrossRef
10.
Zurück zum Zitat Pereira RC, Juppner H, Azucena-Serrano CE, Yadin O, Salusky IB, Wesseling-Perry K (2009) Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease. Bone 45:1161–1168PubMedCrossRef Pereira RC, Juppner H, Azucena-Serrano CE, Yadin O, Salusky IB, Wesseling-Perry K (2009) Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease. Bone 45:1161–1168PubMedCrossRef
11.
Zurück zum Zitat Berndt T, Kumar R (2007) Phosphatonins and the regulation of phosphate homeostasis. Annu Rev Physiol 69:341–359PubMedCrossRef Berndt T, Kumar R (2007) Phosphatonins and the regulation of phosphate homeostasis. Annu Rev Physiol 69:341–359PubMedCrossRef
12.
Zurück zum Zitat Shimada T, Hasegawa H, Yamazaki Y, Muto T, Hino R, Takeuchi Y, Fujita T, Nakahara K, Fukumoto S, Yamashita T (2004) FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. J Bone Miner Res 19:429–435PubMedCrossRef Shimada T, Hasegawa H, Yamazaki Y, Muto T, Hino R, Takeuchi Y, Fujita T, Nakahara K, Fukumoto S, Yamashita T (2004) FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. J Bone Miner Res 19:429–435PubMedCrossRef
13.
Zurück zum Zitat Ben-Dov IZ, Galitzer H, Lavi-Moshayoff V, Goetz R, Kuro-o M, Mohammadi M, Sirkis R, Naveh-Many T, Silver J (2007) The parathyroid is a target organ for FGF23 in rats. J Clin Invest 117:4003–4008PubMed Ben-Dov IZ, Galitzer H, Lavi-Moshayoff V, Goetz R, Kuro-o M, Mohammadi M, Sirkis R, Naveh-Many T, Silver J (2007) The parathyroid is a target organ for FGF23 in rats. J Clin Invest 117:4003–4008PubMed
14.
Zurück zum Zitat Canalejo R, Canalejo A, Martinez-Moreno JM, Rodriguez-Ortiz ME, Estepa JC, Mendoza FJ, Munoz-Castaneda JR, Shalhoub V, Almaden Y, Rodriguez M (2010) FGF23 fails to inhibit uremic parathyroid glands. J Am Soc Nephrol 21:1125–1135PubMedCrossRef Canalejo R, Canalejo A, Martinez-Moreno JM, Rodriguez-Ortiz ME, Estepa JC, Mendoza FJ, Munoz-Castaneda JR, Shalhoub V, Almaden Y, Rodriguez M (2010) FGF23 fails to inhibit uremic parathyroid glands. J Am Soc Nephrol 21:1125–1135PubMedCrossRef
15.
Zurück zum Zitat Gattineni J, Bates C, Twombley K, Dwarakanath V, Robinson ML, Goetz R, Mohammadi M, Baum M (2009) FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Renal Physiol 297:F282–F291PubMedCrossRef Gattineni J, Bates C, Twombley K, Dwarakanath V, Robinson ML, Goetz R, Mohammadi M, Baum M (2009) FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Renal Physiol 297:F282–F291PubMedCrossRef
16.
Zurück zum Zitat Gattineni J, Twombley K, Goetz R, Mohammadi M, Baum M (2011) Regulation of serum 1,25(OH)2 vitamin D3 levels by fibroblast growth factor 23 is mediated by FGF receptors 3 and 4. Am J Physiol Renal Physiol 301:F371–F377PubMedCrossRef Gattineni J, Twombley K, Goetz R, Mohammadi M, Baum M (2011) Regulation of serum 1,25(OH)2 vitamin D3 levels by fibroblast growth factor 23 is mediated by FGF receptors 3 and 4. Am J Physiol Renal Physiol 301:F371–F377PubMedCrossRef
17.
Zurück zum Zitat Urakawa I, Yamazaki Y, Shimada T, Iijima K, Hasegawa H, Okawa K, Fujita T, Fukumoto S, Yamashita T (2006) Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature 444:770–774PubMedCrossRef Urakawa I, Yamazaki Y, Shimada T, Iijima K, Hasegawa H, Okawa K, Fujita T, Fukumoto S, Yamashita T (2006) Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature 444:770–774PubMedCrossRef
19.
Zurück zum Zitat Bonewald L (2007) Osteocytes. In: Marcus DFR, Nelson D, Rosen C (eds) Osteoporosis. Elsevier, Amsterdam, pp 169–190. Bonewald L (2007) Osteocytes. In: Marcus DFR, Nelson D, Rosen C (eds) Osteoporosis. Elsevier, Amsterdam, pp 169–190.
20.
Zurück zum Zitat [No authors listed] (1995) A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. The HYP Consortium. Nat Genet 11:130–136. [No authors listed] (1995) A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. The HYP Consortium. Nat Genet 11:130–136.
21.
Zurück zum Zitat Thompson DL, Sabbagh Y, Tenenhouse HS, Roche PC, Drezner MK, Salisbury JL, Grande JP, Poeschla EM, Kumar R (2002) Ontogeny of Phex/PHEX protein expression in mouse embryo and subcellular localization in osteoblasts. J Bone Miner Res 17:311–320PubMedCrossRef Thompson DL, Sabbagh Y, Tenenhouse HS, Roche PC, Drezner MK, Salisbury JL, Grande JP, Poeschla EM, Kumar R (2002) Ontogeny of Phex/PHEX protein expression in mouse embryo and subcellular localization in osteoblasts. J Bone Miner Res 17:311–320PubMedCrossRef
22.
Zurück zum Zitat Nampei A, Hashimoto J, Hayashida K, Tsuboi H, Shi K, Tsuji I, Miyashita H, Yamada T, Matsukawa N, Matsumoto M, Morimoto S, Ogihara T, Ochi T, Yoshikawa H (2004) Matrix extracellular phosphoglycoprotein (MEPE) is highly expressed in osteocytes in human bone. J Bone Miner Metab 22:176–184PubMedCrossRef Nampei A, Hashimoto J, Hayashida K, Tsuboi H, Shi K, Tsuji I, Miyashita H, Yamada T, Matsukawa N, Matsumoto M, Morimoto S, Ogihara T, Ochi T, Yoshikawa H (2004) Matrix extracellular phosphoglycoprotein (MEPE) is highly expressed in osteocytes in human bone. J Bone Miner Metab 22:176–184PubMedCrossRef
23.
Zurück zum Zitat Rowe PS, Oudet CL, Francis F, Sinding C, Pannetier S, Econs MJ, Strom TM, Meitinger T, Garabedian M, David A, Macher MA, Questiaux E, Popowska E, Pronicka E, Read AP, Mokrzycki A, Glorieux FH, Drezner MK, Hanauer A, Lehrach H, Goulding JN, O’Riordan JL (1997) Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP). Hum Mol Genet 6:539–549PubMedCrossRef Rowe PS, Oudet CL, Francis F, Sinding C, Pannetier S, Econs MJ, Strom TM, Meitinger T, Garabedian M, David A, Macher MA, Questiaux E, Popowska E, Pronicka E, Read AP, Mokrzycki A, Glorieux FH, Drezner MK, Hanauer A, Lehrach H, Goulding JN, O’Riordan JL (1997) Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP). Hum Mol Genet 6:539–549PubMedCrossRef
24.
Zurück zum Zitat Strom TM, Francis F, Lorenz B, Boddrich A, Econs MJ, Lehrach H, Meitinger T (1997) Pex gene deletions in Gy and Hyp mice provide mouse models for X-linked hypophosphatemia. Hum Mol Genet 6:165–171PubMedCrossRef Strom TM, Francis F, Lorenz B, Boddrich A, Econs MJ, Lehrach H, Meitinger T (1997) Pex gene deletions in Gy and Hyp mice provide mouse models for X-linked hypophosphatemia. Hum Mol Genet 6:165–171PubMedCrossRef
25.
Zurück zum Zitat Gowen LC, Petersen DN, Mansolf AL, Qi H, Stock JL, Tkalcevic GT, Simmons HA, Crawford DT, Chidsey-Frink KL, Ke HZ, McNeish JD, Brown TA (2003) Targeted disruption of the osteoblast/osteocyte factor 45 gene (OF45) results in increased bone formation and bone mass. J Biol Chem 278:1998–2007PubMedCrossRef Gowen LC, Petersen DN, Mansolf AL, Qi H, Stock JL, Tkalcevic GT, Simmons HA, Crawford DT, Chidsey-Frink KL, Ke HZ, McNeish JD, Brown TA (2003) Targeted disruption of the osteoblast/osteocyte factor 45 gene (OF45) results in increased bone formation and bone mass. J Biol Chem 278:1998–2007PubMedCrossRef
26.
Zurück zum Zitat Martin A, Liu S, David V, Li H, Karydis A, Feng JQ, Quarles LD (2011) Bone proteins PHEX and DMP1 regulate fibroblastic growth factor Fgf23 expression in osteocytes through a common pathway involving FGF receptor (FGFR) signaling. FASEB J 25:2551–2562PubMedCrossRef Martin A, Liu S, David V, Li H, Karydis A, Feng JQ, Quarles LD (2011) Bone proteins PHEX and DMP1 regulate fibroblastic growth factor Fgf23 expression in osteocytes through a common pathway involving FGF receptor (FGFR) signaling. FASEB J 25:2551–2562PubMedCrossRef
27.
Zurück zum Zitat Rowe PS, Kumagai Y, Gutierrez G, Garrett IR, Blacher R, Rosen D, Cundy J, Navvab S, Chen D, Drezner MK, Quarles LD, Mundy GR (2004) MEPE has the properties of an osteoblastic phosphatonin and minhibin. Bone 34:303–319PubMedCrossRef Rowe PS, Kumagai Y, Gutierrez G, Garrett IR, Blacher R, Rosen D, Cundy J, Navvab S, Chen D, Drezner MK, Quarles LD, Mundy GR (2004) MEPE has the properties of an osteoblastic phosphatonin and minhibin. Bone 34:303–319PubMedCrossRef
28.
Zurück zum Zitat Martin A, David V, Laurence JS, Schwarz PM, Lafer EM, Hedge AM, Rowe PS (2008) Degradation of MEPE, DMP1, and release of SIBLING ASARM-peptides (minhibins): ASARM-peptide(s) are directly responsible for defective mineralization in HYP. Endocrinology 149:1757–1772PubMedCrossRef Martin A, David V, Laurence JS, Schwarz PM, Lafer EM, Hedge AM, Rowe PS (2008) Degradation of MEPE, DMP1, and release of SIBLING ASARM-peptides (minhibins): ASARM-peptide(s) are directly responsible for defective mineralization in HYP. Endocrinology 149:1757–1772PubMedCrossRef
29.
Zurück zum Zitat Rowe PS, Garrett IR, Schwarz PM, Carnes DL, Lafer EM, Mundy GR, Gutierrez GE (2005) Surface plasmon resonance (SPR) confirms that MEPE binds to PHEX via the MEPE-ASARM motif: A model for impaired mineralization in X-linked rickets (HYP). Bone 36:33–46PubMedCrossRef Rowe PS, Garrett IR, Schwarz PM, Carnes DL, Lafer EM, Mundy GR, Gutierrez GE (2005) Surface plasmon resonance (SPR) confirms that MEPE binds to PHEX via the MEPE-ASARM motif: A model for impaired mineralization in X-linked rickets (HYP). Bone 36:33–46PubMedCrossRef
30.
Zurück zum Zitat Addison WN, Nakano Y, Loisel T, Crine P, McKee MD (2008) MEPE–ASARM peptides control extracellular matrix mineralization by binding to hydroxyapatite: An inhibition regulated by PHEX cleavage of ASARM. J Bone Miner Res 23:1638–1649PubMedCrossRef Addison WN, Nakano Y, Loisel T, Crine P, McKee MD (2008) MEPE–ASARM peptides control extracellular matrix mineralization by binding to hydroxyapatite: An inhibition regulated by PHEX cleavage of ASARM. J Bone Miner Res 23:1638–1649PubMedCrossRef
31.
Zurück zum Zitat Liu S, Zhou J, Tang W, Jiang X, Rowe DW, Quarles LD (2006) Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab 291:E38–E49PubMedCrossRef Liu S, Zhou J, Tang W, Jiang X, Rowe DW, Quarles LD (2006) Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab 291:E38–E49PubMedCrossRef
32.
Zurück zum Zitat Woo SM, Rosser J, Dusevich V, Kalajzic I, Bonewald LF (2011) Cell line IDG-SW3 replicates osteoblast-to-late-osteocyte differentiation in vitro and accelerates bone formation in vivo. J Bone Miner Res 26:2634–2646PubMedCrossRef Woo SM, Rosser J, Dusevich V, Kalajzic I, Bonewald LF (2011) Cell line IDG-SW3 replicates osteoblast-to-late-osteocyte differentiation in vitro and accelerates bone formation in vivo. J Bone Miner Res 26:2634–2646PubMedCrossRef
33.
Zurück zum Zitat Lavi-Moshayoff V, Wasserman G, Meir T, Silver J, Naveh-Many T (2010) PTH increases FGF23 gene expression and mediates the high-FGF23 levels of experimental kidney failure: A bone parathyroid feedback loop. Am J Physiol Renal Physiol 299:F882–F889PubMedCrossRef Lavi-Moshayoff V, Wasserman G, Meir T, Silver J, Naveh-Many T (2010) PTH increases FGF23 gene expression and mediates the high-FGF23 levels of experimental kidney failure: A bone parathyroid feedback loop. Am J Physiol Renal Physiol 299:F882–F889PubMedCrossRef
34.
Zurück zum Zitat Rhee Y, Allen MR, Condon K, Lezcano V, Ronda AC, Galli C, Olivos N, Passeri G, O’Brien CA, Bivi N, Plotkin LI, Bellido T (2011) PTH receptor signaling in osteocytes governs periosteal bone formation and intracortical remodeling. J Bone Miner Res 26:1035–1046PubMedCrossRef Rhee Y, Allen MR, Condon K, Lezcano V, Ronda AC, Galli C, Olivos N, Passeri G, O’Brien CA, Bivi N, Plotkin LI, Bellido T (2011) PTH receptor signaling in osteocytes governs periosteal bone formation and intracortical remodeling. J Bone Miner Res 26:1035–1046PubMedCrossRef
35.
Zurück zum Zitat Shimada T, Muto T, Urakawa I, Yoneya T, Yamazaki Y, Okawa K, Takeuchi Y, Fujita T, Fukumoto S, Yamashita T (2002) Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Endocrinology 143:3179–3182PubMedCrossRef Shimada T, Muto T, Urakawa I, Yoneya T, Yamazaki Y, Okawa K, Takeuchi Y, Fujita T, Fukumoto S, Yamashita T (2002) Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Endocrinology 143:3179–3182PubMedCrossRef
36.
Zurück zum Zitat Goetz R, Nakada Y, Hu MC, Kurosu H, Wang L, Nakatani T, Shi M, Eliseenkova AV, Razzaque MS, Moe OW, Kuro-o M, Mohammadi M (2010) Isolated C-terminal tail of FGF23 alleviates hypophosphatemia by inhibiting FGF23-FGFR-Klotho complex formation. Proc Natl Acad Sci USA 107:407–412PubMedCrossRef Goetz R, Nakada Y, Hu MC, Kurosu H, Wang L, Nakatani T, Shi M, Eliseenkova AV, Razzaque MS, Moe OW, Kuro-o M, Mohammadi M (2010) Isolated C-terminal tail of FGF23 alleviates hypophosphatemia by inhibiting FGF23-FGFR-Klotho complex formation. Proc Natl Acad Sci USA 107:407–412PubMedCrossRef
37.
Zurück zum Zitat Farrow EG, Yu X, Summers LJ, Davis SI, Fleet JC, Allen MR, Robling AG, Stayrook KR, Jideonwo V, Magers MJ, Garringer HJ, Vidal R, Chan RJ, Goodwin CB, Hui SL, Peacock M, White KE (2011) Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice. Proc Natl Acad Sci USA 108:E1146–E1155PubMedCrossRef Farrow EG, Yu X, Summers LJ, Davis SI, Fleet JC, Allen MR, Robling AG, Stayrook KR, Jideonwo V, Magers MJ, Garringer HJ, Vidal R, Chan RJ, Goodwin CB, Hui SL, Peacock M, White KE (2011) Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice. Proc Natl Acad Sci USA 108:E1146–E1155PubMedCrossRef
38.
Zurück zum Zitat Bhattacharyya N, Wiench M, Dumitrescu C, Connolly BM, Bugge TH, Patel HV, Gafni RI, Cherman N, Cho M, Hager GL, Collins MT (2012) Mechanism of FGF23 processing in fibrous dysplasia. J Bone Miner Res 27:1132–1141PubMedCrossRef Bhattacharyya N, Wiench M, Dumitrescu C, Connolly BM, Bugge TH, Patel HV, Gafni RI, Cherman N, Cho M, Hager GL, Collins MT (2012) Mechanism of FGF23 processing in fibrous dysplasia. J Bone Miner Res 27:1132–1141PubMedCrossRef
39.
Zurück zum Zitat Liu S, Zhou J, Tang W, Menard R, Feng JQ, Quarles LD (2008) Pathogenic role of Fgf23 in Dmp1-null mice. Am J Physiol Endocrinol Metab 295:E254–E261PubMedCrossRef Liu S, Zhou J, Tang W, Menard R, Feng JQ, Quarles LD (2008) Pathogenic role of Fgf23 in Dmp1-null mice. Am J Physiol Endocrinol Metab 295:E254–E261PubMedCrossRef
40.
Zurück zum Zitat Stubbs JR, He N, Idiculla A, Gillihan R, Liu S, David V, Hong Y, Quarles LD (2011) Longitudinal evaluation of FGF23 changes and mineral metabolism abnormalities in a mouse model of chronic kidney disease. J Bone Miner Res. doi:10.1002/jbmr.516 Stubbs JR, He N, Idiculla A, Gillihan R, Liu S, David V, Hong Y, Quarles LD (2011) Longitudinal evaluation of FGF23 changes and mineral metabolism abnormalities in a mouse model of chronic kidney disease. J Bone Miner Res. doi:10.​1002/​jbmr.​516
41.
Zurück zum Zitat Marsell R, Mirza MA, Mallmin H, Karlsson M, Mellstrom D, Orwoll E, Ohlsson C, Jonsson KB, Ljunggren O, Larsson TE (2009) Relation between fibroblast growth factor-23, body weight and bone mineral density in elderly men. Osteoporos Int 20:1167–1173PubMedCrossRef Marsell R, Mirza MA, Mallmin H, Karlsson M, Mellstrom D, Orwoll E, Ohlsson C, Jonsson KB, Ljunggren O, Larsson TE (2009) Relation between fibroblast growth factor-23, body weight and bone mineral density in elderly men. Osteoporos Int 20:1167–1173PubMedCrossRef
42.
Zurück zum Zitat Hsu HJ, Wu MS (2009) Fibroblast growth factor 23: A possible cause of left ventricular hypertrophy in hemodialysis patients. Am J Med Sci 337:116–122PubMedCrossRef Hsu HJ, Wu MS (2009) Fibroblast growth factor 23: A possible cause of left ventricular hypertrophy in hemodialysis patients. Am J Med Sci 337:116–122PubMedCrossRef
43.
Zurück zum Zitat Mirza MA, Larsson A, Lind L, Larsson TE (2009) Circulating fibroblast growth factor-23 is associated with vascular dysfunction in the community. Atherosclerosis 205:385–390PubMedCrossRef Mirza MA, Larsson A, Lind L, Larsson TE (2009) Circulating fibroblast growth factor-23 is associated with vascular dysfunction in the community. Atherosclerosis 205:385–390PubMedCrossRef
44.
Zurück zum Zitat Mirza MA, Larsson A, Melhus H, Lind L, Larsson TE (2009) Serum intact FGF23 associate with left ventricular mass, hypertrophy and geometry in an elderly population. Atherosclerosis 207:546–551PubMedCrossRef Mirza MA, Larsson A, Melhus H, Lind L, Larsson TE (2009) Serum intact FGF23 associate with left ventricular mass, hypertrophy and geometry in an elderly population. Atherosclerosis 207:546–551PubMedCrossRef
45.
Zurück zum Zitat Gutierrez OM, Wolf M, Taylor EN (2011) Fibroblast growth factor 23, cardiovascular disease risk factors, and phosphorus intake in the health professionals follow-up study. Clin J Am Soc Nephrol 6:2871–2878PubMedCrossRef Gutierrez OM, Wolf M, Taylor EN (2011) Fibroblast growth factor 23, cardiovascular disease risk factors, and phosphorus intake in the health professionals follow-up study. Clin J Am Soc Nephrol 6:2871–2878PubMedCrossRef
46.
Zurück zum Zitat Faul C, Amaral AP, Oskouei B, Hu MC, Sloan A, Isakova T, Gutierrez OM, Aguillon-Prada R, Lincoln J, Hare JM, Mundel P, Morales A, Scialla J, Fischer M, Soliman EZ, Chen J, Go AS, Rosas SE, Nessel L, Townsend RR, Feldman HI, St John Sutton M, Ojo A, Gadegbeku C, Di Marco GS, Reuter S, Kentrup D, Tiemann K, Brand M, Hill JA, Moe OW, Kuro OM, Kusek JW, Keane MG, Wolf M (2011) FGF23 induces left ventricular hypertrophy. J Clin Invest 121:4393–4408PubMedCrossRef Faul C, Amaral AP, Oskouei B, Hu MC, Sloan A, Isakova T, Gutierrez OM, Aguillon-Prada R, Lincoln J, Hare JM, Mundel P, Morales A, Scialla J, Fischer M, Soliman EZ, Chen J, Go AS, Rosas SE, Nessel L, Townsend RR, Feldman HI, St John Sutton M, Ojo A, Gadegbeku C, Di Marco GS, Reuter S, Kentrup D, Tiemann K, Brand M, Hill JA, Moe OW, Kuro OM, Kusek JW, Keane MG, Wolf M (2011) FGF23 induces left ventricular hypertrophy. J Clin Invest 121:4393–4408PubMedCrossRef
47.
Zurück zum Zitat Hughes SE (1997) Differential expression of the fibroblast growth factor receptor (FGFR) multigene family in normal human adult tissues. J Histochem Cytochem 45:1005–1019PubMedCrossRef Hughes SE (1997) Differential expression of the fibroblast growth factor receptor (FGFR) multigene family in normal human adult tissues. J Histochem Cytochem 45:1005–1019PubMedCrossRef
48.
Zurück zum Zitat Takeshita K, Fujimori T, Kurotaki Y, Honjo H, Tsujikawa H, Yasui K, Lee JK, Kamiya K, Kitaichi K, Yamamoto K, Ito M, Kondo T, Iino S, Inden Y, Hirai M, Murohara T, Kodama I, Nabeshima Y (2004) Sinoatrial node dysfunction and early unexpected death of mice with a defect of klotho gene expression. Circulation 109:1776–1782PubMedCrossRef Takeshita K, Fujimori T, Kurotaki Y, Honjo H, Tsujikawa H, Yasui K, Lee JK, Kamiya K, Kitaichi K, Yamamoto K, Ito M, Kondo T, Iino S, Inden Y, Hirai M, Murohara T, Kodama I, Nabeshima Y (2004) Sinoatrial node dysfunction and early unexpected death of mice with a defect of klotho gene expression. Circulation 109:1776–1782PubMedCrossRef
49.
Zurück zum Zitat Li H, Martin A, David V, Quarles LD (2011) Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype. Am J Physiol Endocrinol Metab 300:E508–E517PubMedCrossRef Li H, Martin A, David V, Quarles LD (2011) Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype. Am J Physiol Endocrinol Metab 300:E508–E517PubMedCrossRef
50.
Zurück zum Zitat Desjardins L, Liabeuf S, Renard C, Lenglet A, Lemke HD, Choukroun G, Drueke TB, Massy ZA (2012) FGF23 is independently associated with vascular calcification but not bone mineral density in patients at various CKD stages. Osteoporos Int 23:2017–2025PubMedCrossRef Desjardins L, Liabeuf S, Renard C, Lenglet A, Lemke HD, Choukroun G, Drueke TB, Massy ZA (2012) FGF23 is independently associated with vascular calcification but not bone mineral density in patients at various CKD stages. Osteoporos Int 23:2017–2025PubMedCrossRef
51.
Zurück zum Zitat Dalal M, Sun K, Cappola AR, Ferrucci L, Crasto C, Fried LP, Semba RD (2011) Relationship of serum fibroblast growth factor 23 with cardiovascular disease in older community-dwelling women. Eur J Endocrinol 165:797–803PubMedCrossRef Dalal M, Sun K, Cappola AR, Ferrucci L, Crasto C, Fried LP, Semba RD (2011) Relationship of serum fibroblast growth factor 23 with cardiovascular disease in older community-dwelling women. Eur J Endocrinol 165:797–803PubMedCrossRef
52.
Zurück zum Zitat Stubbs JR, Egwuonwu S (2012) Is fibroblast growth factor 23 a harbinger of mortality in CKD? Pediatr Nephrol 27:697–703PubMedCrossRef Stubbs JR, Egwuonwu S (2012) Is fibroblast growth factor 23 a harbinger of mortality in CKD? Pediatr Nephrol 27:697–703PubMedCrossRef
53.
Zurück zum Zitat Alon US (2011) Clinical practice. Fibroblast growth factor (FGF)23: A new hormone. Eur J Pediatr 170:545–554PubMedCrossRef Alon US (2011) Clinical practice. Fibroblast growth factor (FGF)23: A new hormone. Eur J Pediatr 170:545–554PubMedCrossRef
54.
Zurück zum Zitat Danziger J (2008) The bone-renal axis in early chronic kidney disease: An emerging paradigm. Nephrol Dial Transplant 23:2733–2737PubMedCrossRef Danziger J (2008) The bone-renal axis in early chronic kidney disease: An emerging paradigm. Nephrol Dial Transplant 23:2733–2737PubMedCrossRef
55.
Zurück zum Zitat de Borst MH, Vervloet MG, ter Wee PM, Navis G (2011) Cross talk between the renin–angiotensin–aldosterone system and vitamin D–FGF-23–klotho in chronic kidney disease. J Am Soc Nephrol 22:1603–1609PubMedCrossRef de Borst MH, Vervloet MG, ter Wee PM, Navis G (2011) Cross talk between the renin–angiotensin–aldosterone system and vitamin D–FGF-23–klotho in chronic kidney disease. J Am Soc Nephrol 22:1603–1609PubMedCrossRef
56.
Zurück zum Zitat Aono Y, Yamazaki Y, Yasutake J, Kawata T, Hasegawa H, Urakawa I, Fujita T, Wada M, Yamashita T, Fukumoto S, Shimada T (2009) Therapeutic effects of anti-FGF23 antibodies in hypophosphatemic rickets/osteomalacia. J Bone Miner Res 24:1879–1888PubMedCrossRef Aono Y, Yamazaki Y, Yasutake J, Kawata T, Hasegawa H, Urakawa I, Fujita T, Wada M, Yamashita T, Fukumoto S, Shimada T (2009) Therapeutic effects of anti-FGF23 antibodies in hypophosphatemic rickets/osteomalacia. J Bone Miner Res 24:1879–1888PubMedCrossRef
57.
Zurück zum Zitat Zhang R, Lu Y, Ye L, Yuan B, Yu S, Qin C, Xie Y, Gao T, Drezner MK, Bonewald LF, Feng JQ (2011) Unique roles of phosphorus in endochondral bone formation and osteocyte maturation. J Bone Miner Res 26:1047–1056PubMedCrossRef Zhang R, Lu Y, Ye L, Yuan B, Yu S, Qin C, Xie Y, Gao T, Drezner MK, Bonewald LF, Feng JQ (2011) Unique roles of phosphorus in endochondral bone formation and osteocyte maturation. J Bone Miner Res 26:1047–1056PubMedCrossRef
Metadaten
Titel
FGF23 production by osteocytes
verfasst von
Lynda F. Bonewald
Michael J. Wacker
Publikationsdatum
01.04.2013
Verlag
Springer-Verlag
Erschienen in
Pediatric Nephrology / Ausgabe 4/2013
Print ISSN: 0931-041X
Elektronische ISSN: 1432-198X
DOI
https://doi.org/10.1007/s00467-012-2309-3

Weitere Artikel der Ausgabe 4/2013

Pediatric Nephrology 4/2013 Zur Ausgabe

Update Pädiatrie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.