Sakellariou, Giorgos K., Pearson, Timothy, Lightfoot, Adam P., Nye, Gareth A., Wells, Nicola, Giakoumaki, Ifigeneia I., Vasilaki, Aphrodite, Griffiths, Richard D., Jackson, Malcolm J. and McArdle, Anne (2016) Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy. Scientific Reports, 6. ISSN 2045-2322
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Abstract
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.
Item Type: | Article |
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Additional Information: | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
Uncontrolled Keywords: | ageing,mechanisms of disease |
Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
Related URLs: | |
Depositing User: | Pure Connector |
Date Deposited: | 13 Jan 2017 00:07 |
Last Modified: | 22 Oct 2022 02:07 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/62054 |
DOI: | 10.1038/srep33944 |
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