Redox control of skeletal muscle atrophy.
Open accessAbstract
Skeletal muscles comprise the largest organ system in the body and play an essential role in body movement, breathing, and glucose homeostasis. Skeletal muscle is also an important endocrine organ that contributes to the health of numerous body organs. Therefore, maintaining healthy skeletal muscles is important to support overall health of the body. Prolonged periods of muscle inactivity (e.g., bed rest or limb immobilization) or chronic inflammatory diseases (i.e., cancer, kidney failure, etc.) result in skeletal muscle atrophy. An excessive loss of muscle mass is associated with a poor prognosis in several diseases and significant muscle weakness impairs the quality of life. The skeletal muscle atrophy that occurs in response to inflammatory diseases or prolonged inactivity is often associated with both oxidative and nitrosative stress. In this report, we critically review the experimental evidence that provides support for a causative link between oxidants and muscle atrophy. More specifically, this review will debate the sources of oxidant production in skeletal muscle undergoing atrophy as well as provide a detailed discussion on how reactive oxygen species and reactive nitrogen species modulate the signaling pathways that regulate both protein synthesis and protein breakdown.
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Exercising muscle generates more ROS despite more efficient coupling, and ROS production is not only a marker of mitochondrial dysfunction but also a regulated physiological signal involved in adaptation via redox-sensitive pathways such as PGC-1α, AMPK, and NF-κB.
“This paradox explains why exercising muscle generates more ROS despite more efficient coupling and supports the idea that ROS production is not only a marker of mitochondrial dysfunction, but also a regulated physiological signal, particularly involved in adaptation via redox-sensitive pathways such as PGC-1α, AMPK, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) [32].”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [32]
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Experimental — accuracy not yet measuredOxidative stress inhibits protein synthesis and promotes proteolysis in skeletal muscle.
“Oxidative stress has also been shown to inhibit protein synthesis and promote proteolysis in skeletal muscle [34].”
From Resveratrol prevents sarcopenic obesity by reversing mitochondrial dysfunction and oxidative stress via the PKA/LKB1/AMPK pathway (2019) · cites this paper as [34]
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References 104 · Cited by 207
- Authors
- Powers, S. K., Morton, A. B., Ahn, B., & Smuder, A. J.
- Affiliations
- University of Florida (US)
- Corresponding author
- Powers, Scott K.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2016-09
- Volume
- 98
- Pages
- 208-217
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC5006677
- OpenAlex
- W2283701426
- Cited by
- 207
- References
- 104
- Citations by year
- 2026: 19 · 2025: 29 · 2024: 19 · 2023: 12 · 2022: 14 · 2021: 22 · 2020: 32 · 2019: 20 · 2018: 28 · 2017: 10 · 2016: 2
- FWCI
- 10.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, and Lung Institute (R01 HL-062361, R01 HL-072789, HL-087839)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- skeletal muscle atrophy, redox signaling, reactive oxygen species, reactive nitrogen species, oxidative stress, nitrosative stress, muscle protein synthesis, muscle protein degradation, muscle inactivity, immobilization, chronic inflammation, muscle weakness
- MeSH terms
- Atrophy, Calpain, Humans, Oxidation-Reduction, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, Muscle, Skeletal, Reactive Nitrogen Species, Proteolysis
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