ReviewRespiratory physiology & neurobiology2008
Reactive oxygen species and respiratory plasticity following intermittent hypoxia.
Review in Respiratory physiology & neurobiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
52 citing papers in PubMed, 82 citations in OpenAlex.
- Long-term facilitation of ventilation in humans with chronic spinal cord injury.American journal of respiratory and critical care medicine · 2014Trial
- Long-term facilitation of ventilation following acute continuous hypoxia in awake humans during sustained hypercapnia.The Journal of physiology · 2012Trial
- Progressive augmentation and ventilatory long-term facilitation are enhanced in sleep apnoea patients and are mitigated by antioxidant administration.The Journal of physiology · 2009Trial
- Maximal strength and voluntary activation of adductor pollicis after a single session of acute intermittent hypercapnia or acute intermittent hypoxia.Experimental physiology · 2026Article
- The development but not the maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia requires nucleus tractus solitarii HExperimental neurology · 2025Article
- Neonatal intermittent hypoxemia events are associated with later systemic hypertension.Pediatric research · 2025Article
- Daily acute intermittent hypoxia elicits age & sex-dependent changes in molecules regulating phrenic motor plasticity.Experimental neurology · 2025Article
- Reactive Oxidative Species in Carotid Body Chemoreception: Their Role in Oxygen Sensing and Cardiorespiratory Alterations Induced by Chronic Intermittent Hypoxia.Antioxidants (Basel, Switzerland) · 2025Review
- Mild inflammation impairs acute intermittent hypoxia-induced phrenic long-term facilitation by a spinal adenosine-dependent mechanism.Journal of neurophysiology · 2023Article
- Mechanisms of severe acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 2021Article
- Competing mechanisms of plasticity impair compensatory responses to repetitive apnoea.The Journal of physiology · 2019Article
- Exercise Overrides Blunted Hypoxic Ventilatory Response in Prematurely Born Men.Frontiers in physiology · 2019Article
- Impact of high altitude on key determinants of female reproductive health: a review.International journal of biometeorology · 2018Review
- Intermittent but not sustained moderate hypoxia elicits long-term facilitation of hypoglossal motor output.Respiratory physiology & neurobiology · 2018Article
- Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.The Journal of physiology · 2018Review
- Sphingolipids and Redox Signaling in Renal Regulation and Chronic Kidney Diseases.Antioxidants & redox signaling · 2018Article
- Enhancement of phrenic long-term facilitation following repetitive acute intermittent hypoxia is blocked by the glycolytic inhibitor 2-deoxyglucose.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.Antioxidants & redox signaling · 2016Review
- Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis.Comprehensive Physiology · 2016Review
- Cardiorespiratory events in preterm infants: etiology and monitoring technologies.Journal of perinatology : official journal of the California Perinatal Association · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The neural network controlling breathing exhibits plasticity in response to environmental or physiological challenges. For example, while hypoxia initiates rapid and robust increases in respiratory motor output to defend against hypoxemia, it also triggers persistent changes, or plasticity, in chemosensory neurons and integrative pathways that transmit brainstem respiratory activity to respiratory motor neurons. Frequently studied models of hypoxia-induced respiratory plasticity include: (1) carotid chemosensory plasticity and metaplasticity induced by chronic intermittent hypoxia (CIH), and (2) acute intermittent hypoxia (AIH) induced phrenic long-term facilitation (pLTF) in naïve and CIH preconditioned rats. These forms of plasticity share some mechanistic elements, although they differ in anatomical location and the requirement for CIH preconditioning. Both forms of plasticity require serotonin receptor activation and formation of reactive oxygen species (ROS). While the cellular sources and targets of ROS are not well known, recent evidence suggests that ROS modify the balance of protein phosphatase and kinase activities, shifting the balance towards net phosphorylation and favoring cellular reactions that induce and/or maintain plasticity. Here, we review possible sources of ROS, and the impact of ROS on phosphorylation events relevant to respiratory plasticity.
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What OpenQuestion holds
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.