Alternative Mitochondrial Fuel Extends Life Span

被引：11
|
作者：
Schroeder, Elizabeth A. [1 ,2 ]
Shadel, Gerald S. [1 ,2 ]
机构：
[1] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA
来源：
CELL METABOLISM | 2012年 / 15卷 / 04期
关键词：
INCREASING OXIDATIVE STRESS;
D O I：
10.1016/j.cmet.2012.03.011
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
In this issue of Cell Metabolism, Ristow and colleagues (Zarse et al., 2012) elucidate a conserved mechanism through which reduced insulin-IGF1 signaling activates an AMP-kinase-driven metabolic shift toward oxidative proline metabolism. This, in turn, produces an adaptive mitochondrial ROS signal that extends worm life span. These findings further bolster the concept of mitohormesis as a critical component of conserved aging and longevity pathways.
引用
收藏
页码：417 / 418
页数：2
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