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RETRACTED: Bartlett et al. Uremic Toxins Activates Na/K-ATPase Oxidant Amplification Loop Causing Phenotypic Changes in Adipocytes in In Vitro Models. <i>Int. J. Mol. Sci.</i> 2018, <i>19</i>, 2685.

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脂肪細胞におけるNa/K-ATPaseシグナリングは,動脈硬化を促進する

Bruno S Goncalves, Yaxin Wang, Sneha S Pillai

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    Adipo- NaKtideでアディポサイト Na/ K- ATPase (NKA) を標的にすることで,マウスの動脈硬化が著しく減少しました. このアプローチはまた,代謝の健康を改善し,炎症を軽減し,NKAを心臓代謝疾患の治療目標として強調しました.

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    科学分野:

    • 心血管研究
    • 代謝 疾患
    • 細胞シグナリング

    背景:

    • 脂肪細胞機能障害,酸化ストレス,炎症は代謝障害と動脈硬化に関連しています.
    • Na/K-ATPase (NKA) α1シグナリングはSrcキナーゼを活性化し,酸化ストレスと炎症を促進する.
    • NKA阻害剤であるNaKtideは,体内の全身性酸化ストレスと炎症を軽減する.

    研究 の 目的:

    • 動脈硬化におけるアディポサイト特異的なNKA信号伝達の役割を調査する.
    • 動脈硬化症のマウスモデルにおけるアディポサイトNKAを標的とした治療の可能性を評価する.

    主な方法:

    • アディポ・ナクトイドを用いたアディポ細胞特有のNKA阻害は,アポエ・マウスにおけるレンチウイルスベクトル経由で行われます.
    • 動脈硬化症の誘導は 西洋食で12週間
    • 動脈硬化性プラーク負荷,炎症マーカー,脂肪組織と血における酸化ストレスの評価.

    主要な成果:

    • アディポナキタイドは,大動脈のアーチとシヌスの動脈硬化プラーク領域を著しく減少させた.
    • 動脈硬化病変におけるマクロファージと滑らかな筋肉細胞の減少
    • 脂肪組織の炎症,酸化ストレス,グルコース耐性の改善,全身の炎症の減少

    結論:

    • アディポサイトのNKAシグナル伝達は,動脈硬化症の発達において重要な役割を果たします.
    • 脂肪組織は内分泌および/または副分泌メカニズムを通じてアテロゲネシスに影響を与えます.
    • NKAをターゲットにすることは,心臓代謝疾患の潜在的な治療戦略です.