2011 Fiscal Year Final Research Report
Regulatory mechanisms of mineral homeostasis by FGF23
| Project/Area Number |
21390284
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Endocrinology
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
FUKUMOTO Seiji 東京大学, 医学部・附属病院, 講師 (30202287)
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Keywords | FGF23 / 慢性腎臓病 / くる病 / 骨軟化症 / 抗体 |
|---|
| Research Abstract |
Fibroblast growth factor 23(FGF23) is a hormone that is produced by bone and lowers serum phosphate level by acting mainly on kidney. It has been shown that excess actions of FGF23 cause several kinds of hypophosphatemic rickets/osteomalacia. In addition circulatory FGF23 level was shown to be high in patients with chronic kidney disease(CKD). However, it has been unknown what induces excess actions of FGF23 in patients with hypophosphatemic rickets/osteomalacia and whether high FGF23 in patients with CKD has any significant role in phosphate metabolism. We have reported that mutations in several genes cause hypophosphatemic rickets by increasing serum level of FGF23 and the inhibition of FGF23 activity can improve disease status in a model mouse of hypophosphatemic rickets. Furthermore, increased FGF23 in patients with CKD has been shown to work to prevent the development of hyperphosphatemia. These results indicate that FGf23 has a pivotal role in phosphate metabolism both in healthy people and patients with abnormal phosphate levels.
|
Research Products
(13 results)
-
-
-
-
-
[Journal Article] Therapeutic effect of anti-FGF23 antibodies in hypophosphatemicrickets/osteomalacia2009
Author(s)
Aono Y, Yamazaki Y, Yasutake J, Kawata T, Hasegawa H, Urakawa I, Fujita T, WadaM, Yamashita T, Fukumoto S, Shimada T
-
Journal Title
J Bone Miner Res
Volume: 24
Pages: 1879-1888
Peer Reviewed
-
-
-
-
-
-
-
-
