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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency
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Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency

机译：热量限制导致线粒体生物发生和生物能效率

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摘要

Age-related accumulation of cellular damage and death has been linked to oxidative stress. Calorie restriction (CR) is the most robust, nongenetic intervention that increases lifespan and reduces the rate of aging in a variety of species. Mechanisms responsible for the antiaging effects of CR remain uncertain, but reduction of oxidative stress within mitochondria remains a major focus of research. CR is hypothesized to decrease mitochondrial electron flow and proton leaks to attenuate damage caused by reactive oxygen species. We have focused our research on a related, but different, antiaging mechanism of CR. Specifically, using both in vivo and in vitro analyses, we report that CR reduces oxidative stress at the same time that it stimulates the proliferation of mitochondria through a peroxisome proliferation-activated receptor coactivator 1α signaling pathway. Moreover, mitochondria under CR conditions show less oxygen consumption, reduce membrane potential, and generate less reactive oxygen species than controls, but remarkably they are able to maintain their critical ATP production. In effect, CR can induce a peroxisome proliferation-activated receptor coactivator 1α-dependent increase in mitochondria capable of efficient and balanced bioenergetics to reduce oxidative stress and attenuate age-dependent endogenous oxidative damage.
机译：与年龄有关的细胞损伤和死亡积累与氧化应激有关。热量限制（CR）是最健壮的非遗传干预措施，可以延长寿命并降低各种物种的衰老速率。导致CR抗衰老的机制尚不明确，但线粒体内氧化应激的降低仍是研究的主要重点。假设CR可减少线粒体电子流和质子泄漏，以减轻由活性氧引起的破坏。我们将研究重点放在了相关但不同的CR抗衰老机制上。具体而言，我们使用体内和体外分析，报告说CR降低了氧化应激，同时它通过过氧化物酶体增殖激活受体共激活因子1α信号通路刺激线粒体的增殖。此外，与对照相比，在CR条件下线粒体显示出更少的耗氧量，降低了膜电位并产生了更少的活性氧，但值得注意的是，它们能够维持其关键的ATP产生。实际上，CR可以诱导线粒体中过氧化物酶体增殖激活的受体共激活因子1α依赖性增加，从而有效而平衡地利用生物能降低氧化应激并减弱年龄依赖性内源性氧化损伤。

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