ArticleAntioxidants & redox signaling2011
NADPH oxidase 2 mediates intermittent hypoxia-induced mitochondrial complex I inhibition: relevance to blood pressure changes in rats.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Mechanisms underlying end-organ injury in sleep apnoea.The European respiratory journal · 2026Review
- Advancements in the neurocirculatory reflex response to hypoxia.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Review
- NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle.Redox biology · 2023Article
- Oxidative Stress Response Kinetics after 60 Minutes at Different Levels (10% or 15%) of Normobaric Hypoxia Exposure.International journal of molecular sciences · 2023Article
- Identification of a novel senescence-associated signature to predict biochemical recurrence and immune microenvironment for prostate cancer.Frontiers in immunology · 2023Article
- Adaptive cardiorespiratory changes to chronic continuous and intermittent hypoxia.Handbook of clinical neurology · 2022Review
- 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
- Long-term facilitation of catecholamine secretion from adrenal chromaffin cells of neonatal rats by chronic intermittent hypoxia.Journal of neurophysiology · 2019Article
- Neural Activation of Molecular Circuitry in Intermittent Hypoxia.Current opinion in physiology · 2019Article
- NOX2 oxidase expressed in endosomes promotes cell proliferation and prostate tumour development.Oncotarget · 2018Article
- DNA methylation in the central and efferent limbs of the chemoreflex requires carotid body neural activity.The Journal of physiology · 2018Article
- NADPH oxidase 4 modulates hepatic responses to lipopolysaccharide mediated by Toll-like receptor-4.Scientific reports · 2017Article
- PKA activity exacerbates hypoxia-induced ROS formation and hypoxic injury in PC-12 cells.Toxicology letters · 2017Article
- Epigenetic regulation of redox state mediates persistent cardiorespiratory abnormalities after long-term intermittent hypoxia.The Journal of physiology · 2017Article
- Complement-induced activation of the cardiac NLRP3 inflammasome in sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies identified NADPH oxidases (Nox) and mitochondrial electron transport chain at complex I as major cellular sources of reactive oxygen species (ROS) mediating systemic and cellular responses to intermittent hypoxia (IH). In the present study, we investigated potential interactions between Nox and the mitochondrial complex I and assessed the contribution of mitochondrial ROS in IH-evoked elevation in blood pressure. IH treatment led to stimulus-dependent activation of Nox and inhibition of complex I activity in rat pheochromocytoma (PC)12 cells. After re-oxygenation, Nox activity returned to baseline values within 3 h, whereas the complex I activity remained downregulated even after 24 h. IH-induced complex I inhibition was prevented by Nox inhibitors, Nox2 but not Nox 4 siRNA, in cell cultures and was absent in gp91(phox-/Y) (Nox2 knock-out; KO) mice. Using pharmacological inhibitors, we show that ROS generated by Nox activation mobilizes Ca(2+) flux from the cytosol to mitochondria, leading to S-glutathionylation of 75- and 50-kDa proteins of the complex I and inhibition of complex I activity, which results in elevated mitochondrial ROS. Systemic administration of mito-tempol prevented the sustained but not the acute elevations of blood pressure in IH-treated rats, suggesting that mitochondrial-derived ROS contribute to sustained elevation of blood pressure.
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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.