ArticleThe Journal of physiology2004
Role of oxidative stress in intermittent hypoxia-induced immediate early gene activation in rat PC12 cells.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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Who cites it
66 citing papers in PubMed, 139 citations in OpenAlex.
- Prooxidant/Antioxidant Balance in Hypoxia: A Cross-Over Study on Normobaric vs. Hypobaric "Live High-Train Low".PloS one · 2015Trial
- Losartan abolishes oxidative stress induced by intermittent hypoxia in humans.The Journal of physiology · 2011Trial
- Molecular crosstalk between gas transmitters and catecholamine biosynthesis pathways: a narrative review.Medical gas research · 2027Review
- MeCP2 at the crossroads of hypoxia, oxidative stress, and gene regulation in Rett syndrome.Epigenomics · 2025Review
- Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring.International journal of molecular sciences · 2024Review
- P300/CBP Regulates HIF-1-Dependent Sympathetic Activation and Hypertension by Intermittent Hypoxia.American journal of respiratory cell and molecular biology · 2024Article
- Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome.Signal transduction and targeted therapy · 2023Review
- Experimental Models to Study End-Organ Morbidity in Sleep Apnea: Lessons Learned and Future Directions.International journal of molecular sciences · 2022Review
- Influence of 24 h Simulated Altitude on Red Blood Cell Deformability and Hematological Parameters in Patients with Fontan Circulation.Metabolites · 2022Article
- Protein phosphatase 1 regulates reactive oxygen species-dependent degradation of histone deacetylase 5 by intermittent hypoxia.American journal of physiology. Cell physiology · 2022Article
- Urine and FecalMetabolites · 2022Article
- Chronic and Cycling Hypoxia: Drivers of Cancer Chronic Inflammation through HIF-1 and NF-κB Activation: A Review of the Molecular Mechanisms.International journal of molecular sciences · 2021Review
- Lysine demethylase KDM6B regulates HIF-1α-mediated systemic and cellular responses to intermittent hypoxia.Physiological genomics · 2021Article
- Histone Deacetylase 5 Is an Early Epigenetic Regulator of Intermittent Hypoxia Induced Sympathetic Nerve Activation and Blood Pressure.Frontiers in physiology · 2021Article
- The role of reactive oxygen species in cognitive impairment associated with sleep apnea.Experimental and therapeutic medicine · 2020Article
- Hypoxia-inducible factor-1 mediates pancreatic β-cell dysfunction by intermittent hypoxia.American journal of physiology. Cell physiology · 2020Article
- Hypoxia-inducible factors and obstructive sleep apnea.The Journal of clinical investigation · 2020Review
- Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2020Review
- Article
- Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways.International journal of molecular and cellular medicine · 2020Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Intermittent hypoxia (IH) occurs in many pathophysiological conditions. The molecular mechanisms associated with IH, however, have received little attention. Previous studies have reported that the c-fos gene via formation of activator protein-1 (AP-1) transcription factor contributes to adaptive responses to continuous hypoxia. In the present study, using a cell culture model we examined whether IH activates c-fos and AP-1 and if so, by what mechanisms. Experiments were performed on rat phaeochromocytoma cells exposed to 21% O(2) (normoxia) or 60 and 120 cycles of IH, each cycle consisting 15 s of hypoxia followed by 4 min of normoxia. IH resulted in a significant elevation of c-fos mRNA as well as transcriptional activation. IH was more potent and induced a longer lasting activation of c-fos than comparable cumulative duration of continuous hypoxia. IH increased AP-1 activity and tyrosine hydroxylase (TH) mRNA, an AP-1-regulated downstream gene, and these effects were prevented by antisense c-fos. Superoxide dismutase mimetic, a potent scavenger of superoxide anions, prevented IH-induced c-fos, AP-1 and TH activations. IH increased superoxide anion levels in mitochondria as evidenced by decreased aconitase enzyme activity and increased levels of hydrogen peroxide, a stable dismutated product of superoxide anions. Complex I of the mitochondrial electron transport chain was markedly inhibited in IH exposed cells. Pharmacological inhibitors of complex I mimicked the effects of IH during normoxia and occluded the effects of IH on c-fos activation, suggesting the involvement of the mitochondrial electron transport chain in the generation of superoxide anions during IH. These results suggest IH-induced c-fos-mediated transcriptional activation involves oxidative stress.
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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.