Mitochondria on the fritz? Just…replace them

File this one under “I didn’t see it coming”: Mitochondria can be introduced into cells by simply co-incubating the two, allowing cells with damaged or dysfunctional mitochondria to recover efficient respiration. Since mitochondria accumulate damage with aging, the ability to transfer new mitochondria into aged cells could reverse age-relate decline in energy production, and lift cells out of the vicious cycle whereby oxidative radicals cause mitochondrial damage, which in turn increases the rate of oxidative radical production. From Katrangi et al.:

Xenogenic Transfer of Isolated Murine Mitochondria into Human ρ0 Cells Can Improve Respiratory Function

Mitochondrial DNA mutations are the direct cause of several physiological disorders and are also associated with the aging process. The modest progress made over the past two decades towards manipulating the mitochondrial genome and understanding its function within living mammalian cells means that cures for mitochondrial DNA mutations are still elusive. Here, we report that transformed mammalian cells internalize exogenous isolated mitochondria upon simple co-incubation. We first demonstrate the physical presence of internalized mitochondria within recipient cells using fluorescence microscopy. Second, we show that xenogenic transfer of murine mitochondria into human cells lacking functional mitochondria can functionally restore respiration in cells lacking mtDNA. Third, utilizing the natural competence of isolated mitochondria to take up linear DNA molecules, we demonstrate the feasibility of using cellular internalization of isolated exogenous mitochondria as a potential tool for studying mitochondrial genetics in living mammalian cells.

This is a far cry from introducing mitochondria into intact tissues, but many types of cells can be removed from the body and then re-introduced, so a similar strategy could be employed for bone-marrow or other stem cell populations. Presumably, cells with fresh mitochondria would be more capable of re-growth after re-introduction, possibly pushing out unrepaired cells by outcompeting them for space in stem cell niches.

I’d certainly like to see this repeated in non-transformed cells — transformed cells do all kinds of weird things, after all, and that may well include hyperactive glorping of nearby small particles. The ρ0 experiment goes a fair way toward allaying my skepticism on that subject — cells lacking mitochondria are notoriously sluggish, and if both transformed and ρ0 cells can do something I’m more inclined to believe that all cells can do it — still, if we are to believe that this is a general feature of all cells, I’d like to see a clear demonstration that normal somatic and stem cells are capable of this neat trick.

Note also that the authors introduced murine mitochondria into human cells, apparently without incompatibility; they point out that mitochondria are naturally competent to take up exogenous DNA — i.e., they can be readily engineered. Could we create hybrid human cells with the mitochondria of whales? The anti-doping agencies of the future may have to watch out for souped-up runners with greyhound mitochondria in their muscles…

(Hat tip to Fight Aging!)



  1. Yeah! Better mitochondria! Seriously, let’s just screen for who has the best mitochondria and use theirs instead!

    That being said, I really want to see this repeated. I saw their presentation at Sens3 (i can’t believe i forgot to blog about this talk) and everything seems entirely above board – but it is just so wacky! Can it really be true?

  2. […] Mitochondria on the Fritz? Just…Replace Them – A simple but unexpected discovery – “Mitochondria can be introduced into cells by simply co-incubating the two, allowing cells with damaged or dysfunctional mitochondria to recover efficient respiration.” […]

  3. I want ape mitochondria–gorilla, chimp, or orang–any of the three! I expect the new mites to make me stronger and possibly better at climbing trees. Bonobo mites could lead to more sexual promiscuity, but what the heck?

  4. I am a statin damaged layman with mitochondrial myopathy. There are many of us statin sufferers in this same condition, and this sort of research and reporting give us reason for hope. Thanks for going into the twilight zone. Uh, no bonobo mitos please.

  5. Regarding the comment immediately above, about statin-related damage:

    All statin drugs inhibit HMG-CoA reductase to some extent; unfortunately, the pathways involved in synthesis of coenzyme Q10 are sometimes also compromised. This can result in muscle weakness, with symptoms including but not limited to dyspnea (trouble breathing) and chronic fatigue.

    Recently, several studies have reported improvements in patients who undergo statin cessation and Q10 supplementation, e.g., see here .

    I’m not a medical doctor, but in light of these findings I would recommend exploring dietary Q10 supplementation as a potential remedy — under the guidance of a physician, of course.

    Thanks for your comment, and best of luck.

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