The measurement of reversible redox dependent post-translational modifications and their regulation of mitochondrial and skeletal muscle function
Open accessAbstract
Mitochondrial oxidative stress is a common feature of skeletal myopathies across multiple conditions; however, the mechanism by which it contributes to skeletal muscle dysfunction remains controversial. Oxidative damage to proteins, lipids, and DNA has received the most attention, yet an important role for reversible redox post-translational modifications (PTMs) in pathophysiology is emerging. The possibility that these PTMs can exert dynamic control of muscle function implicates them as a mechanism contributing to skeletal muscle dysfunction in chronic disease. Herein, we discuss the significance of thiol-based redox dependent modifications to mitochondrial, myofibrillar, and excitation-contraction (EC) coupling proteins with an emphasis on how these changes could alter skeletal muscle performance under chronically stressed conditions. A major barrier to a better mechanistic understanding of the role of reversible redox PTMs in muscle function is the technical challenges associated with accurately measuring the changes of site-specific redox PTMs. Here we will critically review current approaches with an emphasis on sample preparation artifacts, quantitation, and specificity. Despite these challenges, the ability to accurately quantify reversible redox PTMs is critical to understanding the mechanisms by which mitochondrial oxidative stress contributes to skeletal muscle dysfunction in chronic diseases.
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Mild oxidative stress acts as a cellular signal that increases skeletal muscle strength, while further increases reduce strength and promote muscle fatigue.
“In deed, the production of mild oxidative stress acts as a cellular signal that increases skeletal muscle strength, while further increases reduce strength and promote muscle fatigue (48).”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [48]
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- Authors
- Kramer, P. A., Duan, J., Qian, W.-J., & Marcinek, D. J.
- Affiliations
- University of Washington (US)
- Pacific Northwest National Laboratory (US)
- Corresponding author
- Marcinek, David J.
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2015-11-25
- Volume
- 6
- Pages
- 347-347
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC4658434
- OpenAlex
- W2184409146
- Cited by
- 54
- References
- 128
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 9 · 2020: 7 · 2019: 4 · 2018: 11 · 2017: 4 · 2016: 5 · 2015: 1
- FWCI
- 0.68
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Physiology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (P01-AG001751, T32-AG000057, P41-GM103493)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitochondrial oxidative stress, skeletal muscle dysfunction, skeletal myopathy, excitation-contraction coupling, myofibrillar proteins, sample preparation artifacts, chronic disease
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