ReviewEuropean biophysics journal : EBJ2005
Acute hypoxia differentially regulates K(+) channels. Implications with respect to cardiac arrhythmia.
Review in European biophysics journal : EBJ, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Therapeutic potential and mechanistic insights of astragaloside IV in the treatment of arrhythmia: a comprehensive review.Frontiers in pharmacology · 2025Review
- Contemporary approach to understand and manage COVID-19-related arrhythmia.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2021Review
- Hypoxic conditioning enhances the angiogenic paracrine activity of human adipose-derived stem cells.Stem cells and development · 2013Article
- Oxygen Sensing, Cardiac Ischemia, HIF-1α and Some Emerging Concepts.Current cardiology reviews · 2010Article
- Contributions of ion channel currents to ventricular action potential changes and induction of early afterdepolarizations during acute hypoxia.Circulation research · 2009Article
- Modulation of K(ATP) currents in rat ventricular myocytes by hypoxia and a redox reaction.Acta pharmacologica Sinica · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The first ion channels demonstrated to be sensitive to changes in oxygen tension were K(+) channels in glomus cells of the carotid body. Since then a number of hypoxia-sensitive ion channels have been identified. However, not all K(+) channels respond to hypoxia alike. This has raised some debate about how cells detect changes in oxygen tension. Because ion channels respond rapidly to hypoxia it has been proposed that the channel is itself an oxygen sensor. However, channel function can also be modified by thiol reducing and oxidizing agents, implicating reactive oxygen species as signals in hypoxic events. Cardiac ion channels can also be modified by hypoxia and redox agents. The rapid and slow components of the delayed rectifier K(+) channel are differentially regulated by hypoxia and beta-adrenergic receptor stimulation. Mutations in the genes that encode the subunits for the channel are associated with Long QT syndrome and sudden cardiac death. The implications with respect to effects of hypoxia on the channel and triggering of cardiac arrhythmia will be discussed.
Indexed as
Identifiers
15726346What OpenQuestion holds
Registered trials
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