ReviewFrontiers in physiology2015
The Measurement of Reversible Redox Dependent Post-translational Modifications and Their Regulation of Mitochondrial and Skeletal Muscle Function.
Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- Mitochondrial oxidative stress in skeletal muscle alters metabolic signaling responses to acute muscle contraction.Free radical biology & medicine · 2026Article
- Mitochondrial bioenergetics in resilience of older adults with gynecologic cancer: design and rationale of a pilot study.GeroScience · 2026Article
- Targeting Sarcopenia in CKD: The Emerging Role of GLP-1 Receptor Agonists.International journal of molecular sciences · 2025Review
- Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches.BMC nephrology · 2025Review
- The correlation between serum alkaline phosphatase and grip strength in middle-aged and elderly people: NHANES 2011-2014.BMC musculoskeletal disorders · 2025Article
- Article
- Protein Oxidative Modifications in Neurodegenerative Diseases: From Advances in Detection and Modelling to Their Use as Disease Biomarkers.Antioxidants (Basel, Switzerland) · 2024Review
- Signatures of Cysteine Oxidation on Muscle Structural and Contractile Proteins Are Associated with Physical Performance and Muscle Function in Older Adults: Study of Muscle, Mobility and Aging (SOMMA).medRxiv : the preprint server for health sciences · 2023Article
- From mitochondria to sarcopenia: role of 17β-estradiol and testosterone.Frontiers in endocrinology · 2023Review
- Article
- High intensity muscle stimulation activates a systemic Nrf2-mediated redox stress response.Free radical biology & medicine · 2021Article
- Characterization of cellular oxidative stress response by stoichiometric redox proteomics.American journal of physiology. Cell physiology · 2021Review
- Tissue Nonspecific Alkaline Phosphatase Function in Bone and Muscle Progenitor Cells: Control of Mitochondrial Respiration and ATP Production.International journal of molecular sciences · 2021Article
- Adult Neural Plasticity in Naked Mole-Rats: Implications of Fossoriality, Longevity and Sociality on the Brain's Capacity for Change.Advances in experimental medicine and biology · 2021Article
- TAK1 preserves skeletal muscle mass and mitochondrial function through redox homeostasis.FASEB bioAdvances · 2020Article
- S-glutathionylation proteome profiling reveals a crucial role of a thioredoxin-like protein in interspecies competition and cariogenecity of Streptococcus mutans.PLoS pathogens · 2020Article
- Protein S-glutathionylation reactions as a global inhibitor of cell metabolism for the desensitization of hydrogen peroxide signals.Redox biology · 2020Review
- SUMOylation in α-Synuclein Homeostasis and Pathology.Frontiers in aging neuroscience · 2020Review
- Post-translational modifications in MeHg-induced neurotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension.Sports (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.