Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy

• Published in: Scientific reports Vol. 6; no. 1; p. 33944
• Main Authors: Sakellariou, Giorgos K, Pearson, Timothy, Lightfoot, Adam P, Nye, Gareth A, Wells, Nicola, Giakoumaki, Ifigeneia I, Vasilaki, Aphrodite, Griffiths, Richard D, Jackson, Malcolm J, McArdle, Anne
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 29.09.2016
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep33944

Age-related loss of skeletal muscle mass and function is a major contributor to morbidity and has a profound effect on the quality of life of older people. The potential role of age-dependent mitochondrial dysfunction and cumulative oxidative stress as the underlying cause of muscle aging remains a controversial topic. Here we show that the pharmacological attenuation of age-related mitochondrial redox changes in muscle with SS31 is associated with some improvements in oxidative damage and mitophagy in muscles of old mice. However, this treatment failed to rescue the age-related muscle fiber atrophy associated with muscle atrophy and weakness. Collectively, these data imply that the muscle mitochondrial redox environment is not a key regulator of muscle fiber atrophy during sarcopenia but may play a key role in the decline of mitochondrial organelle integrity that occurs with muscle aging.