Calorie restriction Decelerating mTOR-driven aging from cells to organisms (including humans)
Calorie restriction Decelerating mTOR-driven aging from cells to organisms (including humans)
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DOI：
10.4161/cc.9.4.10766
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发表时间：
2010-02-15
期刊：
影响因子：
4.3
通讯作者：
Blagosklonny, Mikhail V.
中科院分区：
文献类型：
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作者：
Blagosklonny, Mikhail V.
尽管自 1917 年以来人们就知道热量限制 (CR) 可以延缓衰老，但这个话题仍然存在很大争议。可能是什么原因？在这里我讨论CR的抗衰老作用排除了DNA损伤累积和维护失败作为衰老原因的可能性。相反，它表明衰老部分是由营养感应 TOR（雷帕霉素靶标）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延长到与其他哺乳动物相同的程度。然而，与老鼠不同的是，人类受益于医疗保健，尽管不受限制的个体会加速衰老，但医疗保健可以延长寿命。因此，CR 对人类的影响可能会有所减弱。 CR 到底能延长人类寿命多少？这种延长可以被雷帕霉素等老年抑制剂超越吗？
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?