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2019 Fiscal Year Final Research Report

Development of new treatment in systemic sclerosis by regulating of apelin/APJ signaling

Research Project

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Project/Area Number 17K09968
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Collagenous pathology/Allergology
Research InstitutionGunma University

Principal Investigator

Yokoyama Yoko  群馬大学, 医学部, 技術専門職員 (00241901)

Co-Investigator(Kenkyū-buntansha) 茂木 精一郎  群馬大学, 大学院医学系研究科, 准教授 (20420185)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywords全身性強皮症 / 線維化 / アペリン / 治療 / APJアゴニスト / MM07
Outline of Final Research Achievements

Systemic sclerosis (SSc) is an autoimmune connective tissue disorder characterized by the development of fibrosis in the skin and internal organs as well as by vascular dysfunction.We demonstrated that apelin produced by adipocytes acts as an adipokine inhibit fibrosis of dermal fibroblast and low expression of apelin involve in the pathogenesis of SSc.
We focused APJ agonist MM07 in this experiment. We found that MM07 had greater potential than apelin to inhibit fibrosis of dermal fibroblast and SSc model mouse.

Free Research Field

線維化

Academic Significance and Societal Importance of the Research Achievements

MM07はアペリンとは異なり、APJのバイアス型アゴニストであるため、APJに結合してもAPJは細胞内に取り込まれず、持続してAPJシグナルを活性化させることができる。そして、今回の検討からMM07はアペリンよりも高い線維化抑制効果を示すことがわかった。
全身性強皮症の皮膚線維化抑制をターゲットとする治療薬は少ない。MM07は既にヒトへ投与されており、安全性が示されていることから、強皮症の皮膚線維化に対する臨床応用が期待できる。

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Published: 2021-02-19  

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