University of Copenhagen researchers report in Nature Aging that cardiolipin, a fat molecule in the inner mitochondrial membrane, declines in muscle with age and disease in both mice and humans. Lowering it in young mice shifted muscle fibers from fast-twitch to slow-twitch, mimicking natural aging.
Restoring cardiolipin to about two-thirds of normal levels reversed muscle wasting and prevented premature deaths in the mice. The fiber shift appears to be protective: reactive oxygen species help trigger it and the protein ERRγ coordinates the response. Blocking ERRγ stopped the transition, and antioxidants made the muscles fare worse.
In humans, the study only established that cardiolipin falls with age; the reversal was shown in mice alone. It suggests age-related muscle loss is partly a protective trade-off and points to cardiolipin and ERRγ as possible treatment targets.