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2021 Fiscal Year Final Research Report

The mechanism of increased FGF23 levels in primary hyoperparathyroidism

Research Project

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Project/Area Number 19K08683
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 53040:Nephrology-related
Research InstitutionOsaka City University

Principal Investigator

Yasuo Imanishi  大阪市立大学, 大学院医学研究科, 准教授 (50326253)

Project Period (FY) 2019-04-01 – 2022-03-31
KeywordsFGF23 / リン / PTH / SOST / DMP1
Outline of Final Research Achievements

Fibroblast growth factor 23 (FGF23) secretion is facilitated by the PTH, particularly in hyperparathyroidism. The PTH also attenuates dentin matrix protein 1 (DMP1), which is produced by osteocytes to contribute to bone mineralization and suppress FGF23 expression. The continuous activation of PKA signaling in osteoblasts/osteocytes by sustained PTH can alter gene expression, increase FGF23 expression, and suppress DMP1 expression. In addition, we examined the relationship between FGF23 and sclerostin in PHPT using a mouse model of PHPT and UMR106 mature osteoblast cell line, and found that in PHPT the excessive secretion of PTH leads to increased FGF23 and decreased sclerostin expression in serum and calvaria.

Free Research Field

内分泌学

Academic Significance and Societal Importance of the Research Achievements

原発性副甲状腺機能亢進症(PHPT)における低リン血症の発症機序に、PTHとともにFGF23上昇が寄与しているが、このFGF23上昇機序に骨組織におけるDMP1とSOSTが関与することを示した。本研究によりFGF23分泌調節機構の少なくとも一部が解明された。持続的なリン負荷や高リン血症が、腎機能低下や血管石灰化に関与することが知られており、これらの状態は生命予後悪化の一因となることが知られてる。本研究はFGF23分泌調節機構の解明により、リン負荷や高リン血症の是正における基礎医学的な解決法を示唆するものである。

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Published: 2023-01-30  

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