There are factions within the research community who argue against mitochondrial DNA damage as an important cause of aging. That said, I think I could pick any present hypothesis on the biochemistry of aging and find a faction whose members don't think much of it. For all that the mountains of data cataloging the differences between old tissues and young tissues are largely agreed upon, the field as a whole is a battleground of interpretations over the processes involved in moving from young to old. There are those who think damage akin to wear and tear at a cellular level causes change in metabolism, and those who think that evolved programs of changes in metabolism cause damage. Within the damage-as-root-cause school there are any number of debates over which forms of damage are more important, and which are primary causes of aging versus secondary consequences of other forms of damage.
After a decade following research I more or less agree with the SENS vision of aging and the approach of damage repair. But agreeing with the approach isn't the only reason to back a strategy that aims to repair identified forms of damage that differentiate old tissues from young tissues. The other good reason is that building the various clearly envisaged repair treatments is the fastest way to settle most of the arguments in the field. The past two decades of aging research have demonstrated that it is enormously expensive and very slow to try to figure out what is going on at a cellular and metabolic level in aging. Billions of dollars and thousands of researcher years have not produced any great advance in the big picture consensus: researchers still argue over quite fundamental matters of interpretation despite vast vaults of new data.
So I think it is past time to cut to the chase: implement some of the SENS repair biotechnologies, a task that could be accomplished for a fraction of what has been spent on investigations of calorie restriction alone in the past twenty years. So removal of senescent cells, clearance of metabolic waste, restoration of stem cell populations, destruction of misbehaving immune cells, repair of mitochondrial DNA, and so forth. Try out these technologies in mice: whether or not each type of treatment works, that effort will go a long way towards settling the debate over one particular form of age-related damage. In particular think of arguments over the relevance of mitochondrial DNA damage in aging; if we had a means to repair mitochondrial DNA, and any one of three or four such means is really only a few years distant given a sizable project fund, then there would be no real debate. Either removing the damage works, in the sense of meaningful improvement in measures of health, or it doesn't. There would be far less ambiguity possible after running that experiment a few times.
In any case, here is an open access paper whose authors are not hot on mitochondrial DNA damage in aging. While the mitochondrial theory of aging as originally envisaged is indeed becoming an outmoded viewpoint and is halfway overthrown, rejecting an important role for mitochondrial DNA damage seems like throwing out the baby with the bathwater. It is not hard to argue in opposition to some parts of their position, and I think there's a little of seeing what they want to see going on here. For every paper they could produce to support their points, there are others that undermine them. Mitochondrial dynamics are exceedingly complex, and there is a lot of subtlety in the relationship between mitochondria, generation of oxidative damage, and the possible means by which mitochondrial DNA might become damaged - of which oxidative reactions are but one mechanism. This is why I'd say focus on repair technologies as one of the primary methods of investigation at this time, and cut this Gordian knot - something that these authors would probably agree with, though they envisage an exploration conducted via better ways to induce defined levels and types of mitochondrial DNA damage.
The mitochondrial theory of aging (MTA), a mainstream theory of aging which once included accumulation of mitochondrial DNA (mtDNA) damage by reactive oxygen species (ROS) as its cornerstone, has been increasingly losing ground and is undergoing extensive revision due to its inability to explain a growing body of emerging data. This, in turn, has resulted in both a growing skepticism towards the role of mtDNA mutations in aging, and in the transformation of some of our views on mtDNA, ROS, and aging.
Thus, the increased susceptibility of mtDNA to ROS-induced strand breaks (but not to oxidative base damage) is now viewed as a component of the mitochondria-specific mechanism for the maintenance of mtDNA integrity through abandonment and degradation of severely damaged mtDNA molecules, rather than as a mechanism for accelerated mtDNA mutagenesis. Also, we have begun to appreciate that increased ROS production in aging may represent evidence for adaptive signaling aimed at mitigating detrimental changes, rather than constituting an unwanted but unavoidable byproduct of respiration.
Even though its current status is controversial, it is the MTA that stimulated the research that advanced our understanding of aging and clarified the place of mtDNA in this process. While it is no longer plausible that mtDNA is either the sole or the main determinant of aging, epidemiological studies do still suggest a contribution of mtDNA variation to longevity. Also, it is becoming increasingly obvious that maternally transmitted low levels of germline mtDNA mutations can have a significant impact on health and lifespan. The random genetic drift theory has the potential to reconcile the observed mitochondrial dysfunction in aged organs with the low average levels of mtDNA mutations in some tissues. These and other findings demonstrate that despite dramatic advances, our understanding of the role of mtDNA in aging remains incomplete. This incomplete understanding persists in large part due to our limited ability to manipulate mitochondria in a meaningful way. The lack of approaches to introduce defined base lesions into mtDNA impedes our progress in understanding the specifics of mitochondrial processing of oxidative DNA damage. This, in turn, limits our ability to deconvolute and interpret the spectrum of mtDNA mutations observed in aging.