ArticleAnnals of the New York Academy of Sciences2010
L-type calcium channel as a cardiac oxygen sensor.
Article in Annals of the New York Academy of Sciences, 2010. 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, 16 citations in OpenAlex.
- Regulation of CaCell calcium · 2019Article
- Regulation of CaJournal of molecular and cellular cardiology · 2018Article
- A new method to detect rapid oxygen changes around cells: how quickly do calcium channels sense oxygen in cardiomyocytes?Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Aggravation of myocardial dysfunction by injurious mechanical ventilation in LPS-induced pneumonia in rats.Respiratory research · 2013Article
- Hypoxic regulation of cardiac Ca2+ channel: possible role of haem oxygenase.The Journal of physiology · 2012Article
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Acute oxygen sensing in the heart is thought to occur through redox regulation and phosphorylation of membrane channels. Here we report a novel O2-sensing mechanism involving the C-terminus of the L-type Ca2+ channel and regulated by PKA phosphorylation. In patch-clamped myocytes, oxygen deprivation decreased ICa within 40 s. The suppressive effect of anoxia was relieved by PKA-mediated phosphorylation only when Ca2+ was the charge carrier, whereas phosphorylated IBa remained sensitive to O2 withdrawal. Suppression of Ca2+ release by thapsigargin did not alter the response of ICa to anoxia, suggesting a mandatory role for Ca2+ influx and not Ca2+-induced Ca2+ release (CICR) in O2 regulation of the channel. Consistent with this idea, mutation of 80 amino acids in the Ca2+/CaM-binding domain of the recombinant alpha1C subunit that removes Ca2+ dependent inactivation (CDI) abolished O2 sensitivity of the channel. Our findings suggest that the Ca2+/CaM binding domain of the L-type Ca2+ may represent a molecular site for O2 sensing of the heart.
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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.