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Mitohormesis in Mice via Sustained Basal Activation of Mitochondrial and Antioxidant Signaling

机译：通过持续的线粒体和抗氧化信号传导的基础激活小鼠的模小鼠

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Transient mitochondrial stress can promote beneficial physiological responses and longevity, termed "mitohormesis.'' To interrogate mitohormetic pathways in mammals, we generated mice in which mitochondrial superoxide dismutase 2 (SOD2) can be knocked down in an inducible and reversible manner (iSOD2-KD mice). Depleting SOD2 only during embryonic development did not cause post-natal lethality, allowing us to probe adaptive responses to mitochondrial oxidant stress in adult mice. Liver from adapted mice had increased mitochondrial biogenesis and antioxidant gene expression and fewer reactive oxygen species. Gene expression analysis implicated non-canonical activation of the Nrf2 antioxidant and PPARg/PGC-1a mitochondrial signaling pathways in this response. Transient SOD2 knockdown in embryonic fibroblasts from iSOD2-KD mice also resulted in adaptive mitochondrial changes, enhanced antioxidant capacity, and resistance to a subsequent oxidant challenge. We propose that mitohormesis in response to mitochondrial oxidative stress in mice involves sustained activation of mitochondrial and antioxidant signaling pathways to establish a heightened basal antioxidant state.
机译：短暂的线粒体应激可以促进有益的生理反应和寿命，称为“肠肿术”。为了询问哺乳动物中的细胞侵蚀途径，我们产生的小鼠，其中线粒体超氧化物歧化酶2（SOD2）可以以诱导和可逆的方式敲下来（ISOD2-KD小鼠。仅在胚胎发育期间耗尽SOD2并未引起产后杀伤性致命性，允许我们探测对成人小鼠的线粒体氧化胁迫的适应性反应。来自适应小鼠的肝脏增加了线粒体生物发生和抗氧化基因表达和更少的活性氧。基因表达分析涉及NRF2抗氧化剂和PPARG / PGC-1A线粒体信号传导途径的非规范激活在该响应中。来自ISOD2-KD小鼠的胚胎成纤维细胞的瞬时SOD2敲低也导致适应性的线粒体变化，增强的抗氧化能力和抗性随后的氧化攻击。我们提出了重新中的测量术对小鼠进行线粒体氧化应激的呼吸涉及线粒体和抗氧化信号传导途径的持续活化，以建立高度的基础抗氧化状态。

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