TOR-driven aging Speeding car without brakes
TOR-driven aging Speeding car without brakes
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DOI：
10.4161/cc.8.24.10310
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发表时间：
2009-12-15
期刊：
影响因子：
4.3
通讯作者：
Blagosklonny, Mikhail V.
中科院分区：
文献类型：
--
作者：
Blagosklonny, Mikhail V.
本文讨论了将衰老的有机体与生锈（尽管可以自我修复）的汽车进行传统类比是具有误导性的。真正的比喻是一辆超速行驶的汽车进入低速区域并损坏自身，因为它没有也不可能减速。对于这样一辆没有刹车（实际上没有驾驶员）的汽车来说，永远不会发生生锈老化的情况。本文使用简单的类比（尽管颠倒了老年学），讨论了衰老的起源、mTOR（雷帕霉素靶标）通路的过度激活如何导致衰老、为什么衰老导致损伤（器官损伤）而不是损伤导致衰老、衰老与年龄相关疾病之间的联系、延缓衰老与衰老耐受性以及雷帕霉素抑制衰老。
This article discusses that the traditional analogy of an aging organism with a rusting (albeit self-repairing) car is misleading. The true analogy is a speeding car that enters a low-speed zone and damages itself because it does not and cannot slow down. For such a car without brakes (and actually without a driver), aging from rusting never occurs. Using simple analogies (although turning gerontology upside down), this article discusses the origin of aging, how overactivation of the mTOR (Target of Rapamycin) pathway causes aging, why aging causes damage (organ damage) not damage causes aging, the link between aging and age-related diseases, slow aging versus aging tolerance and suppression of aging with rapamycin.