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The role of throid hormone receptor relating to ER stress response in the kidney.

Research Project

Project/Area Number 15K19451
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Kidney internal medicine
Research InstitutionUniversity of Yamanashi

Principal Investigator

TAKAHASHI Kazuya  山梨大学, 総合研究部, 助教 (00646135)

Research Collaborator FURUYA Fumihiko   (90456450)
KITAMURA Kenichiro   (10304990)
Project Period (FY) 2015-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
KeywordsERストレス / 甲状腺ホルモン受容体 / 慢性腎臓病 / 小胞体ストレス / 腎障害
Outline of Final Research Achievements

There are 13 million chronic kidney disease (CKD) patients and ten thousand of them are required to start dialysis treatment every year in Japan. There is a need to develop curative treatments of CKD. This study was made to reveal the effects of endogenous thyroid hormone receptor (TR) α on the progression of CKD. Therefore we focused on the endoplasmic reticulum stress pathway in the kidney of TRαKO mice with unilateral ureteral obstruction (UUO)-induced kidney injury model for CKD.
Our experimental results suggested that endogenous thyroid hormone receptor α has inhibitory effects on progression of kidney fibrosis.

Report

(3 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report

URL: 

Published: 2015-04-16   Modified: 2018-03-22  

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