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2022 Fiscal Year Final Research Report

Mitochondrial protection in cardiomyocytes by thiosulfate

Research Project

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Project/Area Number 20K09198
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 55050:Anesthesiology-related
Research InstitutionKyushu University

Principal Investigator

TOKUDA Kentaro  九州大学, 大学病院, 助教 (10419567)

Co-Investigator(Kenkyū-buntansha) 赤星 朋比古  九州大学, 医学研究院, 准教授 (20336019)
Project Period (FY) 2020-04-01 – 2023-03-31
Keywordsチオ硫酸 / ドキソルビシン / ミトコンドリア / 心筋障害
Outline of Final Research Achievements

Doxorubicin (DOX) induces cardiac toxicity predominantly due to reactive oxygen species (ROS)-mediated oxidative stress. Previously, we have shown that sodium thiosulfate attenuates DOX-induced cardiotoxicity by suppressing oxidative stress. Based on the finings, we would try to validate the hypothesis if sodium thiosulfate could protect hearts mainly by preserving mitochondrial function in cardiomyocytes. We applied a novel imaging assay Dynamic Nuclear Polirization(DNP)-MRI, which visualizes the redox status in hearts. DNP-MRI revealed that DOX decreased the reduction rates of redox probe in hearts compared to the control. However, it was not shown that sodium thiosulfate attenuated reducing mitochondrial dysfunction in the DOX-induced cardiac dysfunction model. Further research would be needed to solve the hypothesis.

Free Research Field

麻酔科学

Academic Significance and Societal Importance of the Research Achievements

強力な抗がん剤として広く用いられているドキソルビシンは、用量依存性に心筋障害を生じることが知られてお
り、総投与量が制限されることから治療効果として限界がある。我々はこれまでにチオ硫酸ナトリウム投与によって、ドキソルビシンによる心筋障害抑制効果が見られることを示しており、次の段階としてその作用メカニズムの作用点を証明しようとした。残念ながら当初掲げた仮説を証明することはできなかったが、別の作用点を探っていくことで、ドキソルビシンを用いた抗がん剤治療を今後より効果的に行える可能性があると考えられる。

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Published: 2024-01-30  

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