ArticleJournal of cellular physiology2011
Hypoxia-inducible factor 1 mediates increased expression of NADPH oxidase-2 in response to intermittent hypoxia.
Article in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 1 of them a synthesis that pooled it.
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Who cites it
132 citing papers in PubMed, 1 synthesis or guideline pooled it, 200 citations in OpenAlex.
- Cerebral oxidative stress, inflammation and apoptosis induced by intermittent hypoxia: a systematic review and meta-analysis of rodent data.European respiratory review : an official journal of the European Respiratory Society · 2024Pooled it
- Inhibition of TRPC3-Nox2 Complex Formation Ameliorates Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2025Article
- Can Damage to the Rat Lung Induced by Prolonged Normobaric Hypoxia and Norepinephrine Be Reversed by Normoxic Recovery?Current issues in molecular biology · 2025Article
- Green tea's secret weapon: a review on the protective effects of epigallocatechin-3-gallate against ischemia/reperfusion damage.Pharmacological reports : PR · 2025Review
- Oxidative Stress and Inflammation in Hypoxemic Respiratory Diseases and Their Comorbidities: Molecular Insights and Diagnostic Advances in Chronic Obstructive Pulmonary Disease and Sleep Apnea.Antioxidants (Basel, Switzerland) · 2025Review
- Autophagy hub-protein p62 orchestrates oxidative, endoplasmic reticulum stress, and inflammatory responses post-ischemia, exacerbating stroke outcome.Redox biology · 2025Article
- Bayesian-weighted Mendelian randomization reveals sleep apnea syndrome mediates the BMI-chronic pain link.Journal of thoracic disease · 2025Article
- Hypoxia-Induced Reactive Oxygen Species: Their Role in Cancer Resistance and Emerging Therapies to Overcome It.Antioxidants (Basel, Switzerland) · 2025Review
- Mechanisms of microbial infection and wound healing in diabetic foot ulcer: pathogenicity in the inflammatory-proliferative phase, chronicity, and treatment strategies.Frontiers in endocrinology · 2025Review
- Relationship between cognitive dysfunction and urinary 8-OHdG levels in children with obstructive sleep apnea.Frontiers in neurology · 2025Article
- Role of Oxidative Stress in the Occurrence and Development of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea Syndrome.Molecular neurobiology · 2024Review
- The role of ROS in tumor infiltrating immune cells and cancer immunotherapy.Metabolism: clinical and experimental · 2024Review
- Article
- Anemia and Hypoxia Impact on Chronic Kidney Disease Onset and Progression: Review and Updates.Cureus · 2023Review
- The role of hypoxia on prostate cancer progression and metastasis.Molecular biology reports · 2023Review
- Mint3 as a Potential Target for Cooling Down HIF-1α-Mediated Inflammation and Cancer Aggressiveness.Biomedicines · 2023Review
- LncRNAs associated with oxidative stress in diabetic wound healing: Regulatory mechanisms and application prospects.Theranostics · 2023Review
- L-Citrulline Supplementation Reduces Blood Pressure and Myocardial Infarct Size under Chronic Intermittent Hypoxia, a Major Feature of Sleep Apnea Syndrome.Antioxidants (Basel, Switzerland) · 2022Article
- The Role of Inflammation in Cognitive Impairment of Obstructive Sleep Apnea Syndrome.Brain sciences · 2022Review
- The Role of Inflammation, Hypoxia, and Opioid Receptor Expression in Pain Modulation in Patients Suffering from Obstructive Sleep Apnea.International journal of molecular sciences · 2022Review
72 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Sleep-disordered breathing with recurrent apnea is associated with intermittent hypoxia (IH). Cardiovascular morbidities caused by IH are triggered by increased generation of reactive oxygen species (ROS) by pro-oxidant enzymes, especially NADPH oxidase-2 (Nox2). Previous studies showed that (i) IH activates hypoxia-inducible factor 1 (HIF-1) in a ROS-dependent manner and (ii) HIF-1 is required for IH-induced ROS generation, indicating the existence of a feed-forward mechanism. In the present study, using multiple pharmacological and genetic approaches, we investigated whether IH-induced expression of Nox2 is mediated by HIF-1 in the central and peripheral nervous system of mice as well as in cultured cells. IH increased Nox2 mRNA, protein, and enzyme activity in PC12 pheochromocytoma cells as well as in wild-type mouse embryonic fibroblasts (MEFs). This effect was abolished or attenuated by blocking HIF-1 activity through RNA interference or pharmacologic inhibition (digoxin or YC-1) or by genetic knockout of HIF-1α in MEFs. Increasing HIF-1α expression by treating PC 12 cells with the iron chelator deferoxamine for 20 h or by transfecting them with HIF-1alpha expression vector increased Nox2 expression and enzyme activity. Exposure of wild-type mice to IH (8 h/day for 10 days) up-regulated Nox2 mRNA expression in brain cortex, brain stem, and carotid body but not in cerebellum. IH did not induce Nox2 expression in cortex, brainstem, carotid body, or cerebellum of Hif1a(+/-) mice, which do not manifest increased ROS or cardiovascular morbidities in response to IH. These results establish a pathogenic mechanism linking HIF-1, ROS generation, and cardiovascular pathology in response to IH.
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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.