You might recall recent research suggesting that telomere shortening with age is caused by accumulated mitochondrial damage - always promising to see signs that two mechanisms associated with aging might be collapsed into one if you're interested in prevention and repair. Given that plausible methods of repairing mitochondrial damage using the biotechnologies of today are moving closer with each passing year, the more that would be fixed through mitochondrial repair, the better.

With that in mind, Chris Patil notes another possible link:

Why would DNA damage accumulate in aging cells? The trivial explanation is, simply, time passing: Unless repair mechanisms are 100% efficient, the passage of time will result in a slow, steady buildup of damage.

Another possibility is that DNA repair itself becomes less efficient with age, causing damage to accumulate with increasing speed over time. ... in both genomic and mitochondrial DNA, [aged] worms repair their DNA more slowly than young worms

...

The authors propose two speculative causes, the first of which is specific to mitochondrial DNA. Mitochondrial protein targeting and transport become less efficient in aged cells, so even if old cells are synthesizing nuclear-encoded repair enzymes at the same levels as in young cells, these proteins might not make it to their destination, resulting in a decrease in repair activity within the mitochondria.

The second hypothetical cause is more general: ... old cells might lack the energy to perform repair function at maximum efficiency: if ATP is limiting, then simply staying alive will require an increasing proportion of the available energy budget, and the DNA might be allowed to fall into disrepair.

ATP, the cellular fuel supply, is created in the mitochondria, of course. As the mitochondria become more damaged, less ATP is forthcoming - you can see what sort of downward spiral results from the intersection of these facts.

I jest with my fantasy "Mitochondria Did It" model; there's plenty more to the biochemistry of aging that seems very unlikely to be pinned on the ongoing degeneration of mitochondrial function. It is interesting, however, that we see these potential links as the tools of biotechnology grow more effective, and the store of knowledge grows ever larger. Fixing mitochondria looks ever more desirable at the same time as it is becoming ever more plausible.

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