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significance of gnao1 as a novel therapeutic target of heart failure

Research Project

Project/Area Number 19K23963
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeMulti-year Fund
Review Section 0902:General internal medicine and related fields
Research InstitutionKyoto University

Principal Investigator

Inazumi Hideaki  京都大学, 医学研究科, 医員 (10844037)

Project Period (FY) 2019-08-30 – 2021-03-31
Project Status Completed (Fiscal Year 2020)
Budget Amount *help
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords心不全 / Gタンパク
Outline of Research at the Start

本申請研究は、これまで心血管病において注目されていなかった抑制性 G タンパク Gαo の心不全発症・進展における病態生理学的意義を明らかにし、Gαo の新規心不全治療標的としての可能性を示すことである。
具体的には①複数の心不全モデルマウスとGαo ノックアウトマウスとの交配による、Gαo 発現抑制による心不全改善効果の検討、②心筋特異的 Gαo 過剰発現マウス(Gαo-Tg)の表現型解析と内在する分子メカニズムの検討を目指す。

Outline of Final Research Achievements

We revealed that a subtype of inhibitory GTP binding protein Gαo, which role in cardiovascular disease have not been studied before, contributes to the development of heart failure by using multiple mice models of heart failure.

Academic Significance and Societal Importance of the Research Achievements

高齢化に伴い、人口減少にも関わらず今後ますます心不全患者は増加していくことが予想されている。
これまでにも心不全に対する治療薬はいくつか開発されているが未だにその予後は不良であり、心不全の分子メカニズムに基づいた新たな治療標的の発見が望まれている。
本研究により様々な成因からなる心不全の発症、進展に関わる新たな分子メカニズムの一端が明らかになったため、新規心不全治療法の開発に寄与することが期待される。

Report

(3 results)
  • 2020 Annual Research Report   Final Research Report ( PDF )
  • 2019 Research-status Report
  • Research Products

    (7 results)

All 2020 2019

All Presentation (7 results) (of which Int'l Joint Research: 4 results,  Invited: 1 results)

  • [Presentation] CaMK-NRSF-GNAO1 transcriptional circuits participates in the pathological cardiac remodeling2020

    • Author(s)
      Hideaki Inazumi
    • Organizer
      Basic Cardiovascular Science (BCVS) 2020
    • Related Report
      2020 Annual Research Report
    • Int'l Joint Research / Invited
  • [Presentation] Increased Gαo Expression Regulated by NRSF Plays a Key Role in the Development of Heart Failure Through the Impairment of Ca2+ Homeostasis2020

    • Author(s)
      Hideaki Inazumi, Yasuaki Nakagawa, Kenji Moriuchi, Koichiro Kuwahara
    • Organizer
      Basic Cardiovascular Science (BCVS) 2020
    • Related Report
      2020 Annual Research Report
    • Int'l Joint Research
  • [Presentation] NRSF-GNAO1-CaMK2 axis exacerbates cardiac remodeling and progresses heart failure by impairing Ca2+ homeostasis2020

    • Author(s)
      Hideaki Inazumi, Yoshihiro Kuwabara, Koichiro Kuwahara, Yasuaki Nakagawa, Hideyuki Kinoshita, Kenji Moriuchi, Hiromu Yanagisawa, Toshio Nishikimi, Miku Oya, Mitsuhiko Yamada, Toshihide Kashihara, Nagomi Kurebayashi, Masami Sugihara, Kazuwa Nakao , Takeshi Kimura
    • Organizer
      European Society of Cardiology (ESC)
    • Related Report
      2020 Annual Research Report
  • [Presentation] 抑制性G蛋白サブユニットGαoの発現亢進はCa2+ handlingの異常を介して心不全進展にかかわる2019

    • Author(s)
      稲住 英明
    • Organizer
      第56回日本臨床分子医学会学術集会
    • Related Report
      2019 Research-status Report
  • [Presentation] Increased Gαo expression plays a pivotal role in the progression of heart failure by impairing Ca2+ handling2019

    • Author(s)
      Hideaki Inazumi
    • Organizer
      BCVS2019
    • Related Report
      2019 Research-status Report
    • Int'l Joint Research
  • [Presentation] Increased Gαo expression underlies cardiac dysfunction and lethal arrhythmias accompanied with abnormal Ca2+ handling2019

    • Author(s)
      Hideaki Inazumi
    • Organizer
      ESC congress 2019
    • Related Report
      2019 Research-status Report
    • Int'l Joint Research
  • [Presentation] Increased expression of Gαo plays a pivotal role in the progression of heart failure by impairing Ca2+ homeostasis2019

    • Author(s)
      稲住 英明
    • Organizer
      第36回国際心臓研究学会日本部会
    • Related Report
      2019 Research-status Report

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Published: 2019-09-03   Modified: 2022-01-27  

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