Not all researchers are presently convinced that enough evidence exists to place mitochondrial DNA damage front and center as an important cause of aging. I would agree that the tools and measurements discussed below leave some room for argument over what they mean, but at this time the research community is very close to being able to repair mitochondrial DNA, not just talk about it. Thus I think that the best approach for the next few years is to actually go ahead and repair the damage in laboratory animals, and see what happens - that should settle the debate one way or another.
Protection from reactive oxygen species (ROS) and from mitochondrial oxidative damage is well known to be necessary to longevity. The relevance of mitochondrial DNA (mtDNA) to aging is suggested by the fact that the two most commonly measured forms of mtDNA damage, deletions and the oxidatively induced lesion 8-oxo-dG, increase with age. The rate of increase is species-specific and correlates with maximum lifespan.
It is less clear that failure or inadequacies in the protection from reactive oxygen species (ROS) and from mitochondrial oxidative damage are sufficient to explain senescence. DNA containing 8-oxo-dG is repaired by mitochondria, and the high ratio of mitochondrial to nuclear levels of 8-oxo-dG previously reported are now suspected to be due to methodological difficulties. Furthermore, [mice lacking the MnSOD natural antioxidant] incur higher than wild type levels of oxidative damage, but do not display an aging phenotype. Together, these findings suggest that oxidative damage to mitochondria is lower than previously thought, and that higher levels can be tolerated without physiological consequence.
A great deal of work remains before it will be known whether mitochondrial oxidative damage is a "clock" which controls the rate of aging. The increased level of 8-oxo-dG seen with age in isolated mitochondria needs explanation. It could be that a subset of cells lose the ability to protect or repair mitochondria, resulting in their incurring disproportionate levels of damage. Such an uneven distribution could exceed the reserve capacity of these cells and have serious physiological consequences. Measurements of damage need to focus more on distribution, both within tissues and within cells. In addition, study must be given to the incidence and repair of other DNA lesions, and to the possibility that repair varies from species to species, tissue to tissue, and young to old.
In this context, you might also look at the membrane pacemaker theory regarding oxidative damage to mitochondria and longevity differences between species. It places an emphasis on resistance to damage and the consequences of damage over the actual levels of damage.