ArticlePeerJ2013
A non-cardiomyocyte autonomous mechanism of cardioprotection involving the SLO1 BK channel.
Article in PeerJ, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 36 citations in OpenAlex.
- BK Channels Orchestrate Cardiac Homeostasis Through Mitochondrial Uncoupling Proteins.bioRxiv : the preprint server for biology · 2026Article
- The BKPhysiological reports · 2024Article
- Inhibition of BKCell death discovery · 2022Article
- Role and Mechanism of PKC-δ for Cardiovascular Disease: Current Status and Perspective.Frontiers in cardiovascular medicine · 2022Review
- Review
- BK in Double-Membrane Organelles: A Biophysical, Pharmacological, and Functional Survey.Frontiers in physiology · 2021Review
- BKAntioxidants (Basel, Switzerland) · 2020Review
- Optogenetic control of mitochondrial protonmotive force to impact cellular stress resistance.EMBO reports · 2020Article
- Inhibition of BKPhysiological reports · 2018Article
- Expression and Activation of BKFrontiers in cardiovascular medicine · 2018Article
- Preconditioning with the BKAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.The Biochemical journal · 2017Review
- Suppressors of Superoxide-HCell metabolism · 2016Article
- Cardiac Slo2.1 Is Required for Volatile Anesthetic Stimulation of K+ Transport and Anesthetic Preconditioning.Anesthesiology · 2016Article
- The cardioprotective compound cloxyquin uncouples mitochondria and induces autophagy.American journal of physiology. Heart and circulatory physiology · 2016Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- BKCa channel activation increases cardiac contractile recovery following hypothermic ischemia/reperfusion.American journal of physiology. Heart and circulatory physiology · 2015Article
- Closure of mitochondrial potassium channels favors opening of the Tl(+)-induced permeability transition pore in Ca(2+)-loaded rat liver mitochondria.Journal of bioenergetics and biomembranes · 2015Article
- Mitochondrial BKCa channel.Frontiers in physiology · 2015Review
- MaxiK channel and cell signalling.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Opening of BK-type Ca(2+) activated K(+) channels protects the heart against ischemia-reperfusion (IR) injury. However, the location of BK channels responsible for cardioprotection is debated. Herein we confirmed that openers of the SLO1 BK channel, NS1619 and NS11021, were protective in a mouse perfused heart model of IR injury. As anticipated, deletion of the Slo1 gene blocked this protection. However, in an isolated cardiomyocyte model of IR injury, protection by NS1619 and NS11021 was insensitive to Slo1 deletion. These data suggest that protection in intact hearts occurs by a non-cardiomyocyte autonomous, SLO1-dependent, mechanism. In this regard, an in-situ assay of intrinsic cardiac neuronal function (tachycardic response to nicotine) revealed that NS1619 preserved cardiac neurons following IR injury. Furthermore, blockade of synaptic transmission by hexamethonium suppressed cardioprotection by NS1619 in intact hearts. These results suggest that opening SLO1 protects the heart during IR injury, via a mechanism that involves intrinsic cardiac neurons. Cardiac neuronal ion channels may be useful therapeutic targets for eliciting cardioprotection.
Indexed as
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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.