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. Author manuscript; available in PMC: 2013 Mar 12.
Published in final edited form as: Biol Chem. 2012 Dec 1;393(12):1485–1512. doi: 10.1515/hsz-2012-0198

Figure 1. Regulation of mitochondrial quality control and the response to oxidative stress.

Figure 1

An existing mitochondrial population is shown subjected to a pathological stress with the formation of reactive oxygen, nitrogen and lipid species (ROS/RNS/RLS). This oxidative stress damages mtDNA impairing the ability of the organelle to replace damaged electron transport proteins and decreasing bioenergetic reserve capacity; the resulting increased mitochondrial ROS then oxidatively damages previously unmodified mitochondria. The damaged mitochondria are turned over by a mitophagic mechanism that then suppresses this vicious cycle. The mitochondrial population is now renewed through mitochondrial biogenesis. The bioenergetic reserve capacity is essential for resistance to oxidative stress and supplying ATP demand. Once the bioenergetic reserve is depleted, bioenergetic failure occurs and the cell is programmed for cell death.