Scientists at the University of Copenhagen have identified a mitochondrial molecule that may explain why ageing muscles lose strength while activating protective mechanisms against cellular damage.
The study found that declining levels of cardiolipin, a fat molecule essential for mitochondrial function, trigger changes in muscle fibres.
Published findings indicate that cardiolipin levels decline in the muscles of both ageing mice and humans.
Researchers found that reduced cardiolipin levels prompted muscles to shift from fast-twitch fibres, which generate powerful movements, towards slow-twitch fibres associated with endurance.
A protein called ERRγ was found to play a key role in coordinating the changes in muscle fibres.
Scientists at the University of Copenhagen have identified a mitochondrial molecule that may explain why ageing muscles lose strength while activating protective mechanisms against cellular damage.
The study found that declining levels of cardiolipin, a fat molecule essential for mitochondrial function, trigger changes in muscle fibres. Experiments in mice showed that partially restoring the molecule helped reverse muscle wasting and prevented premature deaths in affected animals.
Published findings indicate that cardiolipin levels decline in the muscles of both ageing mice and humans. The molecule supports mitochondrial structure and energy production, making its loss a potential contributor to muscle deterioration.
Researchers found that reduced cardiolipin levels prompted muscles to shift from fast-twitch fibres, which generate powerful movements, towards slow-twitch fibres associated with endurance. Although this transition can reduce strength and speed, it appears to help cells cope with mitochondrial stress.
The team linked this adaptation to reactive oxygen species (ROS), molecules that can damage cells when produced excessively. These molecules also act as signals that activate protective responses. A protein called ERRγ was found to play a key role in coordinating the changes in muscle fibres.
Further experiments revealed that affected muscles absorbed more glucose but redirected much of it towards producing antioxidants rather than generating energy. This response helped protect cells against oxidative damage.
Assistant Professor Fabian Finger, the study’s first and co-corresponding author, said the fibre transition represents a trade-off between power and protection. He cautioned that suppressing ROS with antioxidants worsened muscle outcomes in the experiments.
The findings could open avenues for treating age-related muscle loss, although the therapeutic effects have so far been demonstrated in mice. Researchers are exploring whether restoring cardiolipin or targeting ERRγ could support healthier ageing.
The FDA has granted accelerated approval to elamipretide for Barth syndrome, a rare inherited disorder. However, its effectiveness against ordinary age-related muscle weakness remains uncertain.
