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2019 Fiscal Year Final Research Report

Role of the novel myokine myonectin in regulation of ischemic heart disease

Research Project

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Project/Area Number 17H04175
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Cardiovascular medicine
Research InstitutionNagoya University

Principal Investigator

OUCHI Noriyuki  名古屋大学, 医学系研究科, 寄附講座教授 (00595514)

Co-Investigator(Kenkyū-buntansha) 大橋 浩二  名古屋大学, 医学系研究科, 寄附講座講師 (10595515)
柴田 玲  名古屋大学, 医学系研究科, 寄附講座教授 (70343689)
室原 豊明  名古屋大学, 医学系研究科, 教授 (90299503)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywords虚血性心疾患
Outline of Final Research Achievements

Here we investigated the role of the exercise-induced myokine myonectin in regulation of ischemic heart disease. We found that myonectin knockout mice had increased myocardial infarct size and reduced cardiac function following ischemia-reperfusion compared with control mice, which were accompanied by enhanced apoptosis and inflammatory response in ischemic heart. In contrast, myonectin transgenic mice had reduced ischemia reperfusion injury compared with control mice. Furthermore, myonectin prevented myocardial ischemic injury by reducing cardiomyocyte apoptosis and macrophage inflammatory response through its ability to promote the sphingosine-1-phosphate/cyclicAMP/Akt signaling pathway. Thus, myonectin can function as an exercise-induced myokine which provides cardioprotection.

Free Research Field

循環器内科学

Academic Significance and Societal Importance of the Research Achievements

我が国において虚血性心疾患を代表とする心血管病の病態解明及び治療法の確立は最重要課題である。本研究において、運動誘発性の骨格筋由来分泌因子「マイオカイン」であるマイオネクチンが心筋細胞のアポトーシスとマクロファージの炎症反応の抑制を介して心筋虚血再灌流障害を改善することが明らかとなった。従って、マイオネクチンは心筋保護作用を有するマイオカインでありマイオネクチンを標的とした心血管病の創薬開発が期待される。

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Published: 2021-02-19  

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