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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Free Radic Biol Med. 2015 May 13;85:250–258. doi: 10.1016/j.freeradbiomed.2015.05.005

Figure 1. Proposed mechanisms to explain the role of mtDNA damage to the aging process.

Figure 1

mtDNA mutations can be generated during life or inherited. Both types can accumulate during life, potentially to the point where an OXPHOS defect is generated. This defect may increase superoxide (and other reactive oxygen species) generation, which in theory could further damage the mtDNA. However, experimental evidence of this vicious cycle lacks. Reactive oxygen species are more likely signals triggering protective effects. Recent studies suggest that not only postmitotic cells, but also progenitor cells seem be an important cellular target of mtDNA damage.