Physiological regulation and disorders of phosphate metabolism - Pivotal role of fibroblast growth factor 23

被引:76
作者
Fukumoto, Seiji [1 ]
机构
[1] Tokyo Univ Hosp, Dept Internal Med, Div Nephrol & Endocrinol, Tokyo 113, Japan
关键词
hypophosphatemia; hyperphosphatemia; fibroblast growth factor; Klotho; hormone;
D O I
10.2169/internalmedicine.47.0730
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Fibroblast growth factor (FGF) 23 has been identified as the last member of FGF family. FGF23 reduces serum phosphate level by suppressing proximal tubular phosphate reabsorption and intestinal phosphate absorption. FGF23 is produced by bone and acts on the kidney through a specific receptor system which is composed of Klotho and certain subtypes of FGF receptors. Excess actions of FGF23 cause several hypophosphatemic diseases characterized by impaired renal phosphate reabsorption and rickets/osteomalacia. In contrast, deficient actions of FGF23 result in hyperphosphatemic tumoral calcinosis with enhanced renal phosphate reabsorption. These results indicate that FGF23 works as a hormone to regulate the serum phosphate level.
引用
收藏
页码:337 / 343
页数:7
相关论文
共 51 条
[1]   A novel mutation in fibroblast growth factor 23 gene as a cause of tumoral calcinosis [J].
Araya, K ;
Fukumoto, S ;
Backenroth, R ;
Takeuchi, Y ;
Nakayama, K ;
Ito, N ;
Yoshii, N ;
Yamazaki, Y ;
Yamashita, T ;
Silver, J ;
Igarashi, T ;
Fujita, T .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (10) :5523-5527
[2]  
Badman MK, 2007, CELL METAB, V5, P426, DOI 10.1016/j.cmet.2007.05.002
[3]   Targeted inactivation of Npt2 in mice leads to severe renal phosphate wasting, hypercalciuria, and skeletal abnormalities [J].
Beck, L ;
Karaplis, AC ;
Amizuka, N ;
Hewson, AS ;
Ozawa, H ;
Tenenhouse, HS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (09) :5372-5377
[4]   An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia [J].
Benet-Pagès, A ;
Orlik, P ;
Strom, TM ;
Lorenz-Depiereux, B .
HUMAN MOLECULAR GENETICS, 2005, 14 (03) :385-390
[5]   FGF23 is processed by proprotein convertases but not by PHEX [J].
Beret-Pagès, A ;
Lorenz-Depiereux, B ;
Zischka, H ;
White, KE ;
Econs, MJ ;
Strom, TM .
BONE, 2004, 35 (02) :455-462
[6]   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 [J].
Bergwitz, C ;
Roslin, NM ;
Tieder, M ;
Loredo-Osti, JC ;
Bastepe, M ;
Abu-Zahra, H ;
Frappier, D ;
Burkett, K ;
Carpenter, O ;
Anderson, D ;
Garabédian, M ;
Sermet, I ;
Fujiwara, TM ;
Morgan, K ;
Tenenhouse, HS ;
Jüppner, H .
AMERICAN JOURNAL OF HUMAN GENETICS, 2006, 78 (02) :179-192
[7]   Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism [J].
Feng, Jian Q. ;
Ward, Leanne M. ;
Liu, Shiguang ;
Lu, Yongbo ;
Xie, Yixia ;
Yuan, Baozhi ;
Yu, Xijie ;
Rauch, Frank ;
Davis, Siobhan I. ;
Zhang, Shubin ;
Rios, Hector ;
Drezner, Marc K. ;
Quarles, L. Darryl ;
Bonewald, Lynda F. ;
White, Kenneth E. .
NATURE GENETICS, 2006, 38 (11) :1310-1315
[8]   Most osteomalacia-associated mesenchymal tumors are a single histopathologic entity - An analysis of 32 cases and a comprehensive review of the literature [J].
Folpe, AL ;
Fanburg-Smith, JC ;
Billings, SD ;
Bisceglia, M ;
Bertoni, F ;
Cho, JY ;
Econs, MJ ;
Inwards, CY ;
de Beur, SMJ ;
Mentzel, T ;
Montgomery, E ;
Michal, M ;
Miettinen, M ;
Mills, SE ;
Reith, JD ;
O'Connell, JX ;
Rosenberg, AE ;
Rubin, BP ;
Sweet, DE ;
Vinh, TN ;
Wold, LE ;
Wehrli, BM ;
White, FKE ;
Zaino, RJ ;
Weiss, SW .
AMERICAN JOURNAL OF SURGICAL PATHOLOGY, 2004, 28 (01) :1-30
[9]   A GENE (PEX) WITH HOMOLOGIES TO ENDOPEPTIDASES IS MUTATED IN PATIENTS WITH X-LINKED HYPOPHOSPHATEMIC RICKETS [J].
FRANCIS, F ;
HENNIG, S ;
KORN, B ;
REINHARDT, R ;
DEJONG, P ;
POUSTKA, A ;
LEHRACH, H ;
ROWE, PSN ;
GOULDING, JN ;
SUMMERFIELD, T ;
MOUNTFORD, R ;
READ, AP ;
POPOWSKA, E ;
PRONICKA, E ;
DAVIES, KE ;
ORIORDAN, JLH ;
ECONS, MJ ;
NESBITT, T ;
DREZNER, MK ;
OUDET, C ;
PANNETIER, S ;
HANAUER, A ;
STROM, TM ;
MEINDL, A ;
LORENZ, B ;
CAGNOLI, M ;
MOHNIKE, KL ;
MURKEN, J ;
MEITINGER, T .
NATURE GENETICS, 1995, 11 (02) :130-136
[10]   Hyperostosis-hyperphosphatemia syndrome:: A congenital disorder of O-glycosylation associated with augmented processing of fibroblast growth factor 23 [J].
Frishberg, Yaacov ;
Ito, Nobuaki ;
Rinat, Choni ;
Yamazaki, Yuji ;
Feinstein, Sofia ;
Urakawa, Itaru ;
Navon-Elkan, Paulina ;
Becker-Cohen, Rachel ;
Yamashita, Takeyoshi ;
Araya, Kaori ;
Igarashi, Takashi ;
Fujita, Toshiro ;
Fukumoto, Seiji .
JOURNAL OF BONE AND MINERAL RESEARCH, 2007, 22 (02) :235-242