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首页> 外文期刊>Cell cycle >Calorie restriction: decelerating mTOR-driven aging from cells to organisms (including humans).
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Calorie restriction: decelerating mTOR-driven aging from cells to organisms (including humans).

机译：热量限制：降低mTOR驱动的衰老从细胞到生物体（包括人类）的寿命。

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Although it has been known since 1917 that calorie restriction (CR) decelerates aging, the topic remains highly controversial. What might be the reason? Here I discuss that the anti-aging effect of CR rules out accumulation of DNA damage and failure of maintenance as a cause of aging. Instead, it suggests that aging is driven in part by the nutrient-sensing TOR (target of rapamycin) network. CR deactivates the TOR pathway, thus slowing aging and delaying diseases of aging. Humans are not an exception and CR must increase both maximal and healthy lifespan in humans to the same degree as it does in other mammals. Unlike mice, however, humans benefit from medical care, which prolongs lifespan despite accelerated aging in non-restricted individuals. Therefore in humans the effect of CR may be somewhat blunted. Still how much does CR extend human lifespan? And could this extension be surpassed by gerosuppressants such as rapamycin?
机译：尽管自1917年以来就知道卡路里限制（CR）会减缓衰老，但是这个话题仍然引起很大争议。可能是什么原因？在这里，我讨论了CR的抗衰老作用排除了DNA损伤的积累和维护失败（作为衰老原因）。相反，它表明衰老部分是由营养敏感的TOR（雷帕霉素的靶标）网络驱动的。 CR使TOR通路失活，从而减缓衰老并延缓衰老疾病。人类也不例外，CR必须将人类的最大寿命和健康寿命增加到与其他哺乳动物相同的程度。然而，与小鼠不同，人类受益于医疗服务，尽管非限制性个体的衰老加速，但医疗服务可延长寿命。因此，在人类中，CR的作用可能会减弱。 CR还能延长人类寿命吗？并能被雷帕霉素等Gerosuppressant超越吗？

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