ReviewRespiratory physiology & neurobiology2010
Intermittent hypoxia augments acute hypoxic sensing via HIF-mediated ROS.
Review in Respiratory physiology & neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- The impact of obstructive sleep apnea on skin wound healing - from preclinical perspective to clinical evidence: A narrative review.Sleep & breathing = Schlaf & Atmung · 2026Review
- Article
- Review
- Chemoreflex function in pulmonary diseases - A review.The Journal of physiology · 2025Review
- Possible Molecular Mechanisms of Hypertension Induced by Sleep Apnea Syndrome/Intermittent Hypoxia.Life (Basel, Switzerland) · 2024Review
- Chemogenetic inhibition of NTS astrocytes normalizes cardiac autonomic control and ameliorate hypertension during chronic intermittent hypoxia.Biological research · 2023Article
- Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome.Signal transduction and targeted therapy · 2023Review
- Hydroxytyrosol Alleviated Hypoxia-Mediated PC12 Cell Damage through Activating PI3K/AKT/mTOR-HIF-1Oxidative medicine and cellular longevity · 2022Article
- Lysine demethylase KDM6B regulates HIF-1α-mediated systemic and cellular responses to intermittent hypoxia.Physiological genomics · 2021Article
- Vitamin D Attenuates Hypoxia-Induced Injury in Rat Primary Neuron Cells through Downregulation of the Dual Oxidase 1 (DUOX1) Gene.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Acute and chronic hypoxia differentially predispose lungs for metastases.Scientific reports · 2019Article
- Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension?Frontiers in physiology · 2019Review
- Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- High-performance reoxygenation from PLGA-PEG/PFOB emulsions: a feedback relationship between ROS and HIF-1α.International journal of nanomedicine · 2018Article
- Chronic intermittent hyperoxia alters the development of the hypoxic ventilatory response in neonatal rats.Respiratory physiology & neurobiology · 2016Article
- System for exposing cultured cells to intermittent hypoxia utilizing gas permeable cultureware.General physiology and biophysics · 2015Article
- Endothelial uncoupling protein 2 regulates mitophagy and pulmonary hypertension during intermittent hypoxia.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms.Sleep and biological rhythms · 2015Article
- HIF-1α activation by intermittent hypoxia requires NADPH oxidase stimulation by xanthine oxidase.PloS one · 2015Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Carotid bodies and neonatal adrenal medullary chromaffin cells (AMC) respond rapidly to acute hypoxia before compromising cellular functions. Responses to acute hypoxia are dynamically altered by chronic perturbations in arterial blood O2 levels resulting from breathing disorders. Sleep disordered breathing with recurrent apneas cause periodic decreases in arterial blood O2 or intermittent hypoxia (IH). Recent studies suggest that reactive oxygen species (ROS) mediate cellular adaptations to prolonged hypoxia. In this article we discuss the evidence for ROS in mediating exaggerated carotid body and AMC responses to acute hypoxia by IH and the underlying cellular and molecular mechanisms. IH increases ROS levels, and anti-oxidants prevent IH-induced augmented responses of the carotid body and AMC to hypoxia. The enhanced hypoxic sensitivity by IH involves ROS-dependent recruitment of transmitters/modulators in the carotid body and Ca2+ signaling mechanisms in AMC. Mechanisms by which IH elevates ROS include activation of NADPH oxidases, inhibition of mitochondrial complex I activity and down-regulation of anti-oxidant enzymes. Transcriptional regulation of pro- and anti-oxidant enzymes by hypoxia-inducible factors 1 and 2 appears to be a major molecular mechanism regulating ROS generation by 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.