NATURE:增加自噬延长哺乳动物寿命

2018-05-31 海北 MedSci原创

最近,来自德克萨斯大学西南医学中心的研究人员报告了在基础自噬增加的小鼠模型中,其寿命和健康寿命有所延长。

已有的研究显示,自噬能够增加模型生物的寿命。但是,至今为止,它在促进哺乳动物寿命方面的作用尚未确立。最近,来自德克萨斯大学西南医学中心的研究人员报告了在基础自噬增加的小鼠模型中,其寿命和健康寿命有所延长。

为了确定组成性增加的自噬对哺乳动物健康的影响,研究人员构建了在beclin 1Becn1F121A / F121A)中具有Phe121Ala突变的靶向突变小鼠,降低其与负调节物BCL2的相互作用。研究人员证明beclin 1BCL2之间的相互作用在Becn1F121A / F121A敲入小鼠的几个组织中被毁坏,并带来了较高水平的基础自噬流。

与野生型同窝动物相比,雄性和雌性敲入小鼠的寿命显着增加,年龄相关的肾脏和心脏病变以及自发性肿瘤发生等表型有所减少,敲入小鼠的健康寿命也得到改善。

此外,抗老化蛋白质klotho3缺陷的小鼠中,beclin 1BCL2相互作用有所增加,自噬有所减少。这些表型,以及过早的致命性和不育,能够被beclin 1F121A)突变所拯救。

因此,这些数据表明,破坏beclin 1-BCL2复合物是增加自噬,预防早衰,改善健康状况,并促进哺乳动物寿命的有效机制。


原始出处:
Álvaro F. Fernández et al. Disruption of the beclin 1–BCL2 autophagy regulatory complex promotes longevity in mice. Nature, 2018; DOI: 10.1038/s41586-018-0162-7

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    2018-05-31 明月清辉

    谢谢分享.学习了

    0

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    2018-05-31 飛歌

    学习了很有用

    0

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    2018-05-31 张新亮1853311252142e2fm

    好文献学习了

    0

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    2018-05-31 kafei

    学习学习谢谢

    0

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    2018-05-31 sunfeifeiyang

    学习

    0

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Diabetes:IL-6可通过将自噬与抗氧化反应相偶联从而减少β细胞氧化应激损伤

活性氧(ROS)产生是糖尿病β细胞功能障碍的关键因素。既往研究表明,多效性的细胞因子IL-6与β细胞自噬相关,但IL-6是否影响β细胞的氧化应激尚不明确。Michelle R. Marasco等人利用糖尿病小鼠模型、体外培养的人类胰岛和啮齿动物的β细胞来研究IL-6是否影响氧化应激反应。结果显示IL-6偶联自噬抗氧化应激,可减少β细胞和人类胰岛的ROS。在活体内,β细胞特异性丧失IL-6信号使小鼠