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Revisit of glomerulosclerosis

Research Project

Project/Area Number 17K16100
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Kidney internal medicine
Research InstitutionTokai University

Principal Investigator

KOIZUMI Masahiro  東海大学, 医学部, 講師 (30566170)

Project Period (FY) 2017-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Keywords糸球体硬化症 / 細胞外基質 / Ⅰ型コラーゲン / PHGDH / メサンギウム細胞 / 糸球体線維化 / I型コラーゲン / 質量分析計 / 質量分析 / 線維化 / ポドサイト / 質量分析法
Outline of Final Research Achievements

We examined a hypothesis that glomerulosclerosis induced transformation of type 1 collagen fromα1(I)2α2(I) heterotrimer toα1(I)3 homotrimer, but were not able to prove this hypothesis in the analysis using mass spectrometry. However, in the comprehensive analysis of the changes in sclerosed glomeruli, the levels of PHGDH, which is a rate-limiting enzyme in glycine biosynthesis pathway, was significantly increased. This amino acid is a major component of collagen. This result indicated that this pathway plays an important role in the pathogenesis and development of glomerulosclerosis.

Academic Significance and Societal Importance of the Research Achievements

当初の仮説を立証することは出来なかったが,質量分析による検討から糸球体硬化症の発症機序に関し「硬化糸球体ではPHGDH産生が亢進し,この酵素を阻害することにより糸球体硬化症が軽減する」という新たな仮説の着想に至った.この仮説に基づいた研究はコラーゲンの主構成アミノ酸glycineの産生経路に着目したユニークなものであり,不可逆的な病態で現時点で有効な治療が確立されていない糸球体硬化症の新規治療法の開発に繋がることが期待される.

Report

(4 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Research-status Report
  • 2017 Research-status Report
  • Research Products

    (6 results)

All 2019 2018 2017

All Journal Article (1 results) (of which Int'l Joint Research: 1 results,  Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (5 results) (of which Int'l Joint Research: 2 results,  Invited: 1 results)

  • [Journal Article] Podocyte Injury Augments Intrarenal Angiotensin II Generation and Sodium Retention in a Megalin-Dependent Manner2019

    • Author(s)
      Koizumi Masahiro、Ueda Kohei、Niimura Fumio、Nishiyama Akira、Yanagita Motoko、Saito Akihiko、Pastan Ira、Fujita Toshiro、Fukagawa Masafumi、Matsusaka Taiji
    • Journal Title

      Hypertension

      Volume: 74 Issue: 3 Pages: 509-517

    • DOI

      10.1161/hypertensionaha.118.12352

    • Related Report
      2019 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research
  • [Presentation] 腎内Angiotensin IIのポドサイト傷害時の病態形成における役割2018

    • Author(s)
      小泉賢洋
    • Organizer
      高血圧関連疾患モデル学会学術総会
    • Related Report
      2018 Research-status Report
    • Invited
  • [Presentation] Podocyte injury enhances intrarenal Angiotensin II generation and sodium retention dependently on megalin2018

    • Author(s)
      Masahiro Koizumi
    • Organizer
      Gordon Research Seminar
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research
  • [Presentation] ポドサイト傷害後にmegalin依存性に増加した腎内Angiotensin IIは浮腫形成に寄与する2017

    • Author(s)
      小泉賢洋
    • Organizer
      日本腎臓学会学術集会
    • Related Report
      2017 Research-status Report
  • [Presentation] 腎内Angiotensin IIのポドサイト傷害時の病態形成における役割2017

    • Author(s)
      小泉賢洋
    • Organizer
      日本高血圧学会学術集会
    • Related Report
      2017 Research-status Report
  • [Presentation] Podocyte injury enhances intrarenal Angiotensin II generation and sodium retention dependently on megalin2017

    • Author(s)
      Masahiro Koizumi
    • Organizer
      American Society of Nephrology
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research

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Published: 2017-04-28   Modified: 2021-02-19  

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