Bear in mind that the evolution of aging is anything but a settled field. It is a battleground of many competing views and theories. The evolution of aging is one of those topics for which the wikipedia page is actually a good place to start, because right from the top it correctly delivers the understanding that this field is (a) complicated, (b) not at all unified, and (c) in flux.

https://en.wikipedia.org/wiki/Evolution_of_ageing

The fellow here is outlining one particular set of views out of something like half a dozen with varying degrees of mainstream support, and that any random selection of evolutionary biologists would take issue with, point by point. He also simplifies down to a level at which some important points are missed, such as the existence of mitochondrially targeted antioxidants and what their ability to slow aging means for various theories of aging and mitochondrial function.

In fact all of the appearances of mitochondria in this article are in that bucket of missing important but subtle points. If you want to chase down more on the viewpoint he discusses in the last section of the article, you should read up on the membrane pacemaker hypothesis:

https://www.google.com/#q=Membrane+Pacemaker+Hypothesis

This is really driven by trying to understand why the outliers on the chart of resting metabolic rate versus species life span are outliers: naked mole rats, birds, microbats, etc.

When it comes to what to do about damaged, bad mitochondria in aging, there are better options than replacement. In fact delivery of good mitochondria as a therapy is probably not useful at all; the bad mitochondria already outcompeted the good mitochondria once, and will quickly do so again. It is so rapid that scientists have never observed this in progress, they only see cells with all bad mitochondria and cells without any bad mitochondria, never the transitional state.

(There are two separate things going on in aging vis a vis mitochondria. Firstly the type of damage to mitochondria that results in bad mitochondria, under discussion here. Secondly changes in cell signaling and environment that leads to a sort of general malaise in mitochondrial function and replication thoughout a tissue without this damage or formation of bad mitochondria, and that is not really under discussion here or in the article. It is probably a secondary consequence of other forms of damage and change in aging).

The SENS approach of allotopic expression, moving mitochondrial genes into the cell nucleus, currently demonstrated for three of the necessary thirteen genes, is the best and most permanent of solutions to prevent mitochondrial damage, being a one-time therapy. If something else is used, such as periodic delivery of replacement mitochondria, it would have to coupled with some kind of targeted destruction of bad mitochondria. That is a thorny problem, as anything less than complete destruction is just a short postponement. These things replicate quickly, and bad mitochondria of the aging-causing sort have a replication advantage over normal, good mitochondria. I'm not aware of anyone with a credible approach to that selective destruction yet, however.