Actions and mode of actions of FGF19 subfamily members

被引:104
作者
Fukumoto, Seiji [1 ]
机构
[1] Tokyo Univ Hosp, Dept Med, Div Nephrol & Endocrinol, Bunkyo Ku, Tokyo 1138655, Japan
关键词
hypophosphatemia; hyperphosphatemia; klotho; FGF;
D O I
10.1507/endocrj.KR07E-002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Fibroblast growth factors (FGFs) are Immoral factors with diverse biological functions. While most FGFs were shown to work as local factors regulating cell growth and differentiation, recent investigations indicated that FGF19 subfamily members, FGF15/19, FGF21 and FGF23 work as systemic factors. FGF 15/19 produced by intestine inhibits bile acid synthesis and FGF21 from liver is involved in carbohydrate and lipid metabolism. In addition, FGF23 was shown to be produced by bone and regulate phosphate and vitamin D metabolism. Furthermore, these FGFs require klotho or beta klotho for their actions in addition to canonical FGF receptors. It is possible that these FGFs together with their receptor systems might be targets for novel therapeutic measures in the future.
引用
收藏
页码:23 / 31
页数:9
相关论文
共 52 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]   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
[4]   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
[5]   The β-glucuronidase klotho hydrolyzes and activates the TRPV5 channel [J].
Chang, Q ;
Hoefs, S ;
van der Kemp, AW ;
Topala, CN ;
Bindels, RJ ;
Hoenderop, JG .
SCIENCE, 2005, 310 (5747) :490-493
[6]   Identification of a hormonal basis for gallbladder filling [J].
Choi, Mihwa ;
Moschetta, Antonio ;
Bookout, Angie L. ;
Peng, Li ;
Umetani, Michihisa ;
Holmstrom, Sam R. ;
Suino-Powell, Kelly ;
Xu, H. Eric ;
Richardson, James A. ;
Gerard, Robert D. ;
Mangelsdorf, David J. ;
Kliewer, Steven A. .
NATURE MEDICINE, 2006, 12 (11) :1253-1255
[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]   Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men [J].
Ferrari, SL ;
Bonjour, JP ;
Rizzoli, R .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (03) :1519-1524
[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