Alternative mitochondrial fuel extends life span.

Departments of Pathology and Genetics, Yale University School of Medicine, New Haven, CT 06520-8023, USA.
Cell metabolism (Impact Factor: 17.35). 04/2012; 15(4):417-8. DOI: 10.1016/j.cmet.2012.03.011
Source: PubMed

ABSTRACT 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.

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