Departments of Pathology and Genetics, Yale University School of Medicine, New Haven, CT 06520-8023, USA.
Cell Metab. 2012 Apr 4;15(4):417-8. doi: 10.1016/j.cmet.2012.03.011.
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.
在本期《细胞代谢》中，Ristow 及其同事（Zarse 等人，2012 年）阐明了一个保守的机制，即降低胰岛素-IGF1 信号通过 AMP 激酶驱动的代谢转变为氧化脯氨酸代谢，从而产生适应性的线粒体 ROS 信号，延长蠕虫的寿命。这些发现进一步支持了线粒体激素作为保守的衰老和长寿途径的关键组成部分的概念。
