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.
Highlights
We33,34 and others[35,36] have recently reported that pharmacological application of the mitochondria-targeted SS31 tetrapeptide can attenuate mitochondrial superoxide production in intact mitochondria of skeletal muscle fibers
In order to define whether a fiber type specificity in muscle atrophy existed, anterior tibialis (AT) cross sections were immunolabeled for the 4 myosin heavy chain (MHC) isoforms (Fig. 1e)
These findings confirm that age-related loss of muscle mass at 28 mo is strongly associated with the reduction in fiber size irrespective of fiber type, these data are derived from studies of a muscle predominantly composed of type II fibers
Summary
We33,34 and others[35,36] have recently reported that pharmacological application of the mitochondria-targeted SS31 tetrapeptide can attenuate mitochondrial superoxide production in intact mitochondria of skeletal muscle fibers This pharmacological approach complements genetic approaches, including those using targeted overexpression of the human catalase gene to mitochondria (MCat mice)[2,23]. The purpose of the present study was to determine the effect of the mitochondria-targeted SS31 peptide on redox homeostasis in muscles of old mice, including mitochondrial ROS (mtROS) and oxidative damage, mitochondrial content and mitophagy and on age-related muscle atrophy and weakness. This work has identified that the age-related changes in mitochondrial redox potential play a key role in the loss of mitochondrial organelle integrity that occurs with aging, but are not involved in the processes of age-related muscle fiber atrophy
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