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Deletion of NAD(P)H Oxidase 2 Prevents Angiotensin II-Induced Skeletal Muscle Atrophy


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タイトル: Deletion of NAD(P)H Oxidase 2 Prevents Angiotensin II-Induced Skeletal Muscle Atrophy
著者: Kadoguchi, Tomoyasu 著作を一覧する
Takada, Shingo 著作を一覧する
Yokota, Takashi 著作を一覧する
Furihata, Takaaki 著作を一覧する
Matsumoto, Junichi 著作を一覧する
Tsuda, Masaya 著作を一覧する
Mizushima, Wataru 著作を一覧する
Fukushima, Arata 著作を一覧する
Okita, Koichi 著作を一覧する
Kinugawa, Shintaro 著作を一覧する
発行日: 2018年 1月 2日
出版者: Hindawi
誌名: BioMed Research International
巻: 2018
開始ページ: 3194917
出版社 DOI: 10.1155/2018/3194917
抄録: Skeletal muscle atrophy is induced by an imbalance between protein synthesis and degradation. Our previous studies reported that angiotensin II (AII) directly induced muscle atrophy in mice. This study investigated the role of NAD(P)H oxidase 2 (Nox2) activation by AII in the induction of skeletal muscle atrophy. For 4 weeks, either saline (vehicle: V) or AII (1000 ng kg(-1) min(-1)) was infused into male wild-type (WT) and Nox2 knockout (KO) mice via osmotic minipumps. Experiments were performed in the following 4 groups: WT + V, KO + V, WT + AII, and KO + AII. Body weight, muscle weight, and myocyte cross-sectional area were significantly decreased in WT + AII compared to WT + V mice, and these changes were not observed in KO + AII mice. Akt phosphorylation of Ser473 and p70S6K of Thr389 was decreased, gene expression levels of MuRF-1 and atrogin-1 were increased in WT + AII compared to WT + V, and these changes were significantly attenuated in KO + AII mice. The deletion of Nox2 prevented AII-induced skeletal muscle atrophy via improving the balance between protein synthesis and degradation. Therefore, Nox2 may be a therapeutic target for AII-induced skeletal muscle atrophy.
資料タイプ: article
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 絹川 真太郎


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