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

Giorgos K. Sakellariou; Timothy Pearson; Adam P. Lightfoot; Gareth A. Nye; Nicola Wells; Ifigeneia I. Giakoumaki; Aphrodite Vasilaki; Richard D. Griffiths; Malcolm J. Jackson; Anne McArdle

doi:10.1038/srep33944

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

Giorgos K. Sakellariou, Timothy Pearson, Adam P. Lightfoot, Gareth A. Nye, Nicola Wells, Ifigeneia I. Giakoumaki, Aphrodite Vasilaki, Richard D. Griffiths, Malcolm J. Jackson, Anne McArdle

Research output: Contribution to journal › Article › peer-review

96 Citations (Scopus)

18 Downloads (Pure)

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.

Original language	English
Article number	33944
Journal	Scientific Reports
Volume	6
DOIs	https://doi.org/10.1038/srep33944
Publication status	Published - 29 Sep 2016

Keywords

Ageing
Mechanisms of disease

Access to Document

10.1038/srep33944Licence: CC BY

Published manuscript
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/
Final published version, 2.34 MB

http://www.nature.com/articles/srep33944

Cite this

@article{4a8c51500f444ca1b7b3299adc62c31e,

title = "Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy",

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.",

keywords = "Ageing, Mechanisms of disease",

author = "Sakellariou, {Giorgos K.} and Timothy Pearson and Lightfoot, {Adam P.} and Nye, {Gareth A.} and Nicola Wells and Giakoumaki, {Ifigeneia I.} and Aphrodite Vasilaki and Griffiths, {Richard D.} and Jackson, {Malcolm J.} and Anne McArdle",

note = "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{\textquoteright}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/",

year = "2016",

month = sep,

day = "29",

doi = "10.1038/srep33944",

language = "English",

volume = "6",

journal = "Scientific Reports",

issn = "2045-2322",

publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy

AU - Sakellariou, Giorgos K.

AU - Pearson, Timothy

AU - Lightfoot, Adam P.

AU - Nye, Gareth A.

AU - Wells, Nicola

AU - Giakoumaki, Ifigeneia I.

AU - Vasilaki, Aphrodite

AU - Griffiths, Richard D.

AU - Jackson, Malcolm J.

AU - McArdle, Anne

N1 - 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/

PY - 2016/9/29

Y1 - 2016/9/29

N2 - 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.

AB - 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.

KW - Ageing

KW - Mechanisms of disease

U2 - 10.1038/srep33944

DO - 10.1038/srep33944

M3 - Article

VL - 6

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 33944

ER -