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2020 Fiscal Year Final Research Report

Pathophysiological analysis of a mitochondrial protein MAIP1 in NASH/NAFLD.

Research Project

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Project/Area Number 18K06656
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 47030:Pharmaceutical hygiene and biochemistry-related
Research InstitutionOsaka University

Principal Investigator

SAKAI EIKO (小河英子)  大阪大学, 薬学研究科, 特任研究員 (60359859)

Project Period (FY) 2018-04-01 – 2021-03-31
Keywords肝臓 / 脂質 / 酸化ストレス / マイクロRNA
Outline of Final Research Achievements

We have previously identified a novel target gene of miR-27b, MAIP1. miR-27b is reported to be unregulated in NASH NAFLD patients. Also we have shown that knockdown of MAIP1 in a cultured hepatocarcinoma cell line induced lipid accumulation as well as down-regulation of oxidative phosphorylations. In this study, we observed that knockdown of MAIP1 resulted in defects of a variety of mitochondrial functions, such as membrane potentials, oxygen consumption rate of complex 1, resulting in increased ROS production and increased lesion in mitochondria genomes. These results suggested potential contribution of decreased MAIP1 expression in NASH/NAFLD.

Free Research Field

分子生物学

Academic Significance and Societal Importance of the Research Achievements

本研究により、MAIP1の発現低下が脂質蓄積だけではなくミトコンドリア機能の低下および酸化ストレスの発生を誘導することを明らかとした。さらに、その原因として電子伝達系機能の阻害があることを示した。これにより、NAHS/NAFLD病態に対して、ミトコンドリア機能の抑制と酸化ストレスを介してMAIP1が寄与する可能性を示した。これらの知見はMAIP1を標的とした創薬・治療法の開発に向けた基盤をなることが期待される。

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Published: 2022-01-27  

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