Many means of breaking cell biology can produce things that look superficially like accelerated aging in at least some ways. That doesn't mean it is aging: given that aging is widespread tissue dysfunction, anything that causes widespread tissue dysfunction can have overlapping phenotypes, but that doesn't mean it has anything to do with normal aging. DNA repair deficiency is the usual example - something that isn't all that apparent in normal aging, in comparison to the models in which DNA repair machinery is missing or broken.
So, similarly, pulling the rug out from under mitochondrial function can be done in countless ways that have very little to do with what happens in aging. I think the onus is still on these researchers to demonstrate that the method they have chosen has much of anything to do with aging per se.