Restoring cardiolipin reverses muscle wasting in mice — SkimNews
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- Cardiolipin levels drop in muscle mitochondria from both aging mice and aging humans, accompanied by structural abnormalities in the mitochondria and a loss of normal function.
- University of Copenhagen researchers reproduced the aging pattern in young mice by experimentally lowering cardiolipin, pushing muscle fibers from the fast-twitch type toward slow-twitch.
- Restoring cardiolipin to approximately two-thirds of its normal concentration began reversing muscle wasting and completely prevented the premature deaths seen in the affected animals.
- ERRγ coordinates the response — inhibiting it in lab-grown muscle cells stopped the fiber-type transition entirely, while the reactive oxygen species unleashed by low cardiolipin help initiate that switch.
- Glucose taken up by mice with insufficient cardiolipin was redirected toward manufacturing their own antioxidants rather than producing energy, with labeled-sugar tracing showing the extra fuel was not burned for power.
- Antioxidants backfired in these mice: as Assistant Professor Fabian Finger put it, the fiber switch is "the muscle trading power for protection," so mopping up reactive oxygen species left their muscles "fared worse, not better."
- Elamipretide, a medication designed to stabilize cardiolipin, recently received FDA accelerated approval for Barth syndrome, showing the target is medically feasible — though the therapeutic results here came from mice, with human samples used only to confirm age-related cardiolipin decline.
Why it matters: For people with age-related muscle loss, the finding reframes weakness as an active defense rather than passive decay: in mice, restoring cardiolipin to about two-thirds of normal reversed wasting, while antioxidants made muscles fare worse. ERRγ's nuclear-receptor family is already targeted by roughly 10-15% of FDA-approved small-molecule medicines.
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