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TOR 驱动的衰老:没有刹车的飞驰汽车。

TOR-driven aging: speeding car without brakes.

机构信息

Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, Buffalo, NY, USA.

出版信息

Cell Cycle. 2009 Dec 15;8(24):4055-9. doi: 10.4161/cc.8.24.10310. Epub 2009 Dec 9.

DOI:10.4161/cc.8.24.10310
PMID:19923900
Abstract

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.

摘要

本文讨论了将衰老的生物体比作生锈(尽管可以自我修复)的汽车这一传统比喻是具有误导性的。真正的比喻是一辆高速行驶的汽车进入低速区并自行损坏,因为它不能也无法减速。对于这样一辆没有刹车(实际上也没有司机)的汽车来说,生锈导致的衰老永远不会发生。本文使用简单的类比(尽管颠覆了老年学的观点),讨论了衰老的起源,mTOR(雷帕霉素靶蛋白)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,衰老与与年龄相关的疾病之间的联系,减缓衰老与衰老耐受以及用雷帕霉素抑制衰老。

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