Figure 3.
Current models for mitochondrial longevity. Inhibition of ETC function can lead to increased level of ROS (red circles), which can induce lifespan extension. One effect of this ROS production is stabilization of the hypoxia-inducible transcription factor HIF-1 and activation of the intrinsic apoptotic pathway. Protein misfolding in the mitochondria causes induction of the UPRmt and inhibition of translation by the kinase GCN-2. This concerted mechanisms promotes protein homeostasis in the mitochondria. Other factors have also been implicated in lifespan extension following inhibition of mitochondrial function including AMPK, the homebox protein CEH-23, the p53 homolog CEP-1, and other transcription and signaling factors.