Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy
Authors
Nye, GarethSakellariou, Giorgos
Pearson, Timothy
Lightfoot, Adam
Wells, Nicola
Giakoumaki, Ifigeneia
Vasilaki, Aphrodite
Griffiths, Richard
Jackson, Malcolm
McArdle, Anne
Affiliation
University of LiverpoolPublication Date
2016-09-29
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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.Citation
Sakellariou, G., Pearson, T., Lightfoot, A., Nye, G., Wells, N., Giakoumaki, I., . . . McArdle, A. (2016). Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy. Scientific Reports, 6(1), 33944Publisher
Nature ResearchJournal
Scientific ReportsAdditional Links
https://www.nature.com/articles/srep33944Type
ArticleLanguage
enEISSN
2045-2322ae974a485f413a2113503eed53cd6c53
10.1038/srep33944
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Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-nd/4.0/