A recent example of research in which researchers break the mitochondrial biochemistry of mice and then reverse that breakage is doing the rounds in the press, being pitched as a reversal of aging. It is not a reversal of aging, however, and I’d say that the researchers involved still have to prove that the particular breakage that they engineered is in fact relevant in normal aging. The appearance of similar outcomes between the breakage and aging does not mean that it is relevant.
Why is this the case? Aging is an accumulation of specific forms of biochemical damage that leads to widespread tissue dysfunction. Given that, the outcome of any form of damage that leads to widespread tissue dysfunction inevitably shares some appearances with normal aging. Since that outcome results from entirely different root causes, however, it is of little relevance or use to developing a better understanding of aging. Mammalian biochemistry can be severely broken and damaged in a near infinite number of ways that do not occur in aging to any significant degree, which is why one has to read the details carefully when this sort of work is published. The media never gets it right.