ReviewJournal of applied physiology (Bethesda, Md. : 1985)2015
Redox regulation of muscle adaptations to contractile activity and aging.
Review in Journal of applied physiology (Bethesda, Md. : 1985), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Trial
- Aging is associated with altered estrogen receptor expression and alters redox protein balance in human female skeletal muscle.GeroScience · 2026Article
- Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs.The FEBS journal · 2026Article
- Critical role of mitochondrial aconitase in skeletal muscle maturation.Scientific reports · 2025Article
- Skeletal muscle innervation: Reactive oxygen species as regulators of neuromuscular junction dynamics and motor unit remodeling.Free radical biology & medicine · 2025Review
- Mitochondrial dysfunction in age-related sarcopenia: mechanistic insights, diagnostic advances, and therapeutic prospects.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023Review
- Article
- The Potential Modulatory Effects of Exercise on Skeletal Muscle Redox Status in Chronic Kidney Disease.International journal of molecular sciences · 2023Review
- Redox-related biomarkers in physical exercise.Redox biology · 2021Review
- Superoxide-mediated oxidative stress accelerates skeletal muscle atrophy by synchronous activation of proteolytic systems.GeroScience · 2020Article
- Sarcopenia: Molecular Pathways and Potential Targets for Intervention.International journal of molecular sciences · 2020Review
- Article
- Exercise, redox homeostasis and the epigenetic landscape.Redox biology · 2020Review
- Reactive oxygen species (ROS) as pleiotropic physiological signalling agents.Nature reviews. Molecular cell biology · 2020Review
- Piceatannol markedly upregulates heme oxygenase-1 expression and alleviates oxidative stress in skeletal muscle cells.Biochemistry and biophysics reports · 2019Article
- Stay Fit, Stay Young: Mitochondria in Movement: The Role of Exercise in the New Mitochondrial Paradigm.Oxidative medicine and cellular longevity · 2019Review
- Antioxidants in Personalized Nutrition and Exercise.Advances in nutrition (Bethesda, Md.) · 2018Review
- Relation of nNOS isoforms to mitochondrial density and PGC-1alpha expression in striated muscles of mice.Nitric oxide : biology and chemistry · 2018Article
- Skeletal Muscle Pyruvate Dehydrogenase Phosphorylation and Lactate Accumulation During Sprint Exercise in Normoxia and Severe Acute Hypoxia: Effects of Antioxidants.Frontiers in physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Superoxide and nitric oxide are generated by skeletal muscle, and these species are increased by contractile activity. Mitochondria have long been assumed to play the primary role in generation of superoxide in muscle, but recent studies indicate that, during contractile activity, membrane-localized NADPH oxidase(s) rapidly generate(s) superoxide that plays a role in redox signaling. This process is important in upregulation of rapid and specific cytoprotective responses that aid maintenance of cell viability following contractile activity, but the overall extent to which redox signaling contributes to regulation of muscle metabolism and homeostasis following contractile activity is currently unclear, as is identification of key redox-sensitive protein targets involved in these processes. Reactive oxygen and nitrogen species have also been implicated in the loss of muscle mass and function that occurs with aging, although recent work has questioned whether oxidative damage plays a key role in these processes. A failure of redox signaling occurs in muscle during aging and may contribute to the age-related loss of muscle fibers. Whether such changes in redox signaling reflect primary age-related changes or are secondary to the fundamental mechanisms is unclear. For instance, denervated muscle fibers within muscles from aged rodents or humans appear to generate large amounts of mitochondrial hydrogen peroxide that could influence adjacent innervated fibers. Thus, in this instance, a "secondary" source of reactive oxygen species may be potentially generated as a result of a primary age-related pathology (loss of neurons), but, nevertheless, may contribute to loss of muscle mass and function during aging.
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What OpenQuestion holds
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.