ArticleFrontiers in physiology2016
NOX2 Inhibition Impairs Early Muscle Gene Expression Induced by a Single Exercise Bout.
Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
- Impact of single anaerobic exercise on delayed activation of endothelial xanthine oxidase in men and women.Redox report : communications in free radical research · 2017Trial
- The effect of exercise-intensity on skeletal muscle stress kinase and insulin protein signaling.PloS one · 2017Trial
- Mitochondrial oxidative stress in skeletal muscle alters metabolic signaling responses to acute muscle contraction.Free radical biology & medicine · 2026Article
- Enzyme-Specific Redox Stability and Plasticity in Trained Youth Athletes: Longitudinal Analysis of SOD and GPX.International journal of molecular sciences · 2026Article
- Dysferlin and the Regulation of CaCells · 2025Review
- Metformin suppresses the mitochondrial and transcriptional response to exercise, revealing a conserved BCL6B-associated angiogenic program.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Alterations in FoxO3a, NF-κB, and MuRF1 Expression in the Soleus Muscle of Male Rats Following High-Intensity Interval Training and Detraining.Doklady. Biochemistry and biophysics · 2024Article
- Reactive oxygen species promote endurance exercise-induced adaptations in skeletal muscles.Journal of sport and health science · 2024Review
- Review
- NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle.Redox biology · 2023Article
- The mediating role of inflammaging between mitochondrial dysfunction and sarcopenia in aging: a review.American journal of clinical and experimental immunology · 2023Review
- Potential Role of Chronic Physical Exercise as a Treatment in the Development of Vitiligo.Frontiers in physiology · 2022Article
- Article
- Effective Accentuation of Voltage-Gated Sodium Current Caused by Apocynin (4'-Hydroxy-3'-methoxyacetophenone), a Known NADPH-Oxidase Inhibitor.Biomedicines · 2021Article
- Exercise-Stimulated ROS Sensitive Signaling Pathways in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2021Review
- Nox2 Inhibition Regulates Stress Response and Mitigates Skeletal Muscle Fiber Atrophy during Simulated Microgravity.International journal of molecular sciences · 2021Article
- How N-Acetylcysteine Supplementation Affects Redox Regulation, Especially at Mitohormesis and Sarcohormesis Level: Current Perspective.Antioxidants (Basel, Switzerland) · 2021Review
- Redox basis of exercise physiology.Redox biology · 2020Review
- Compartmentalized muscle redox signals controlling exercise metabolism - Current state, future challenges.Redox biology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) participate as signaling molecules in response to exercise in skeletal muscle. However, the source of ROS and the molecular mechanisms involved in these phenomena are still not completely understood. The aim of this work was to study the role of skeletal muscle NADPH oxidase isoform 2 (NOX2) in the molecular response to physical exercise in skeletal muscle. BALB/c mice, pre-treated with a NOX2 inhibitor, apocynin, (3 mg/kg) or vehicle for 3 days, were swim-exercised for 60 min. Phospho-p47(phox) levels were significantly upregulated by exercise in flexor digitorum brevis (FDB). Moreover, exercise significantly increased NOX2 complex assembly (p47(phox)-gp91(phox) interaction) demonstrated by both proximity ligation assay and co-immunoprecipitation. Exercise-induced NOX2 activation was completely inhibited by apocynin treatment. As expected, exercise increased the mRNA levels of manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx), citrate synthase (CS), mitochondrial transcription factor A (tfam) and interleukin-6 (IL-I6) in FDB muscles. Moreover, the apocynin treatment was associated to a reduced activation of p38 MAP kinase, ERK 1/2, and NF-κB signaling pathways after a single bout of exercise. Additionally, the increase in plasma IL-6 elicited by exercise was decreased in apocynin-treated mice compared with the exercised vehicle-group (p < 0.001). These results were corroborated using gp91-dstat in an in vitro exercise model. In conclusion, NOX2 inhibition by both apocynin and gp91dstat, alters the intracellular signaling to exercise and electrical stimuli in skeletal muscle, suggesting that NOX2 plays a critical role in molecular response to an acute exercise.
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Registered trials
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