ArticleNature communications2019
Cytosolic ROS production by NADPH oxidase 2 regulates muscle glucose uptake during exercise.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 2 of them syntheses that pooled it.
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
107 citing papers in PubMed, 2 syntheses or guidelines pooled it, 210 citations in OpenAlex.
- Pooled it
- Effects of Mitoquinone (MitoQ) Supplementation on Aerobic Exercise Performance and Oxidative Damage: A Systematic Review and Meta-analysis.Sports medicine - open · 2024Pooled it
- Trial
- Oxidative eustress is associated with AMPK and AKT activation, GLUT4 translocation and glucose uptake in skeletal muscle cells and fibres.Redox report : communications in free radical research · 2026Article
- A quantitative redox proteome of the human muscle response to exercise.bioRxiv : the preprint server for biology · 2026Article
- NOX2-Driven Oxidative Stress and Endothelial Dysfunction in Male Elite Adolescent Soccer Players.Biomolecules · 2026Article
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Systems modelling of mitochondrial dynamics in different exercise regimes.The Journal of physiology · 2026Article
- Spatiotemporal analysis of reactive oxygen species using specific activity-based sensing fluorescent imaging probes.Nature reviews. Chemistry · 2026Review
- Exercise Training Stimulates the Release of Glutathione Peroxidase 1 (GPX1)-Enriched Extracellular Vesicles That Promote Angiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- A decline in skeletal muscle NOX4 abrogates exercise-induced adaptive homeostasis and exacerbates biological aging.Science advances · 2026Article
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Update: Is exercise-induced oxidative stress a friend or foe?Sports medicine and health science · 2026Review
- Molecular Biomarkers of Training Responses: A Systems Framework for Exercise Adaptation and Athlete Monitoring.International journal of molecular sciences · 2026Review
- Metabolic Adaptation during Cardiac Exercise Rehabilitation in Patients after a First Myocardial Infarction.Journal of proteome research · 2026Article
- The impact of exercise on brain mitochondrial health and its relevance to Alzheimer's disease.Brain and environment · 2026Article
- Detecting oxidants in muscleRedox biochemistry and chemistry · 2026Article
- Insulin resistance: mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Flow Cytometric Methods for ROS Quantification in Skeletal Muscle Myotubes.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Redox regulation in aging muscles: exercise as a key modulator to combat sarcopenia and frailty.Frontiers in cell and developmental biology · 2026Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) act as intracellular compartmentalized second messengers, mediating metabolic stress-adaptation. In skeletal muscle fibers, ROS have been suggested to stimulate glucose transporter 4 (GLUT4)-dependent glucose transport during artificially evoked contraction ex vivo, but whether myocellular ROS production is stimulated by in vivo exercise to control metabolism is unclear. Here, we combined exercise in humans and mice with fluorescent dyes, genetically-encoded biosensors, and NADPH oxidase 2 (NOX2) loss-of-function models to demonstrate that NOX2 is the main source of cytosolic ROS during moderate-intensity exercise in skeletal muscle. Furthermore, two NOX2 loss-of-function mouse models lacking either p47phox or Rac1 presented striking phenotypic similarities, including greatly reduced exercise-stimulated glucose uptake and GLUT4 translocation. These findings indicate that NOX2 is a major myocellular ROS source, regulating glucose transport capacity during moderate-intensity exercise.
Indexed as
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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.