ReviewRespiratory physiology & neurobiology2007
The role of NADPH oxidase in carotid body arterial chemoreceptors.
Review in Respiratory physiology & neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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.
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Who cites it
16 citing papers in PubMed, 37 citations in OpenAlex.
- The role of hydrogen sulphide in the control of breathing in hypoxic zebrafish (Danio rerio).The Journal of physiology · 2014Article
- Modulation of K2P3.1 (TASK-1), K2P9.1 (TASK-3), and TASK-1/3 heteromer by reactive oxygen species.Pflugers Archiv : European journal of physiology · 2012Article
- Tetrodotoxin as a tool to elucidate sensory transduction mechanisms: the case for the arterial chemoreceptors of the carotid body.Marine drugs · 2011Review
- Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor-Ca2+ release channel by NADPH oxidase 4.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Adenosine A₂a receptors and O₂ sensing in development.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Serotonin 2A and 2B receptor-induced phrenic motor facilitation: differential requirement for spinal NADPH oxidase activity.Neuroscience · 2011Article
- Intermittent hypoxia augments acute hypoxic sensing via HIF-mediated ROS.Respiratory physiology & neurobiology · 2010Review
- Redox modulation of the fetal cardiovascular defence to hypoxaemia.The Journal of physiology · 2010Article
- Modulation of chronic hypoxia-induced chemoreceptor hypersensitivity by NADPH oxidase subunits in rat carotid body.Journal of applied physiology (Bethesda, Md. : 1985) · 2010Article
- Episodic spinal serotonin receptor activation elicits long-lasting phrenic motor facilitation by an NADPH oxidase-dependent mechanism.The Journal of physiology · 2009Article
- NADPH oxidase activity is necessary for acute intermittent hypoxia-induced phrenic long-term facilitation.The Journal of physiology · 2009Review
- NADPH oxidase is required for the sensory plasticity of the carotid body by chronic intermittent hypoxia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Exposure to cyclic intermittent hypoxia increases expression of functional NMDA receptors in the rat carotid body.Journal of applied physiology (Bethesda, Md. : 1985) · 2009Article
- Reactive oxygen species and respiratory plasticity following intermittent hypoxia.Respiratory physiology & neurobiology · 2008Review
- Respiratory plasticity after perinatal hyperoxia is not prevented by antioxidant supplementation.Respiratory physiology & neurobiology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
O(2)-sensing in the carotid body occurs in neuroectoderm-derived type I glomus cells where hypoxia elicits a complex chemotransduction cascade involving membrane depolarization, Ca(2+) entry and the release of excitatory neurotransmitters. Efforts to understand the exquisite O(2)-sensitivity of these cells currently focus on the coupling between local P(O2) and the open-closed state of K(+)-channels. Amongst multiple competing hypotheses is the notion that K(+)-channel activity is mediated by a phagocytic-like multisubunit enzyme, NADPH oxidase, which produces reactive oxygen species (ROS) in proportion to the prevailing P(O2). In O(2)-sensitive cells of lung neuroepithelial bodies (NEB), multiple studies confirm that ROS levels decrease in hypoxia, and that E(M) and K(+)-channel activity are indeed controlled by ROS produced by NADPH oxidase. However, recent studies in our laboratories suggest that ROS generated by a non-phagocyte isoform of the oxidase are important contributors to chemotransduction, but that their role in type I cells differs fundamentally from the mechanism utilized by NEB chemoreceptors. Data indicate that in response to hypoxia, NADPH oxidase activity is increased in type I cells, and further, that increased ROS levels generated in response to low-O(2) facilitate cell repolarization via specific subsets of K(+)-channels.
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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.