ArticlePloS one2014
KCNMA1 encoded cardiac BK channels afford protection against ischemia-reperfusion injury.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 97 citations in OpenAlex.
- Klotho Deficiency Impairs Distal Potassium Homeostasis Through mTORC1-Dependent Suppression of ROMK.Acta physiologica (Oxford, England) · 2026Article
- BK Channels Orchestrate Cardiac Homeostasis Through Mitochondrial Uncoupling Proteins.bioRxiv : the preprint server for biology · 2026Article
- Polydopamine-Based Antioxidant Countermeasures Against Spaceflight-Induced Neurodegeneration.Small science · 2026Article
- Cytochrome C-like Domain Within the Human BK Channel.International journal of molecular sciences · 2025Article
- Small Molecule NS11021 Promotes BK Channel Activation by Increasing Inner Pore Hydration.Journal of chemical information and modeling · 2024Article
- Loss of the large conductance calcium-activated potassium channel causes an increase in mitochondrial reactive oxygen species in glioblastoma cells.Pflugers Archiv : European journal of physiology · 2023Article
- External Hemin as an Inhibitor of Mitochondrial Large-Conductance Calcium-Activated Potassium Channel Activity.International journal of molecular sciences · 2022Article
- Luteolin-Induced Activation of Mitochondrial BKAntioxidants (Basel, Switzerland) · 2022Article
- Inhibition of BKCell death discovery · 2022Article
- Ion Transport and Radioresistance.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Epigenome-Wide Association Study Reveals Differential Methylation Sites and Association of Gene Expression Regulation with Ischemic Moyamoya Disease in Adults.Oxidative medicine and cellular longevity · 2022Article
- Role and Mechanism of PKC-δ for Cardiovascular Disease: Current Status and Perspective.Frontiers in cardiovascular medicine · 2022Review
- Regulatory mechanisms of mitochondrial BKChannels (Austin, Tex.) · 2021Review
- Mitochondrial ion channels in cardiac function.American journal of physiology. Cell physiology · 2021Review
- Routes for Potassium Ions across Mitochondrial Membranes: A Biophysical Point of View with Special Focus on the ATP-Sensitive KBiomolecules · 2021Review
- Review
- Single channel properties of mitochondrial large conductance potassium channel formed by BK-VEDEC splice variant.Scientific reports · 2021Article
- BK in Double-Membrane Organelles: A Biophysical, Pharmacological, and Functional Survey.Frontiers in physiology · 2021Review
- BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke.Frontiers in cellular neuroscience · 2021Article
- BKAntioxidants (Basel, Switzerland) · 2020Review
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Authors and funding
21 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial potassium channels have been implicated in myocardial protection mediated through pre-/postconditioning. Compounds that open the Ca2+- and voltage-activated potassium channel of big-conductance (BK) have a pre-conditioning-like effect on survival of cardiomyocytes after ischemia/reperfusion injury. Recently, mitochondrial BK channels (mitoBKs) in cardiomyocytes were implicated as infarct-limiting factors that derive directly from the KCNMA1 gene encoding for canonical BKs usually present at the plasma membrane of cells. However, some studies challenged these cardio-protective roles of mitoBKs. Herein, we present electrophysiological evidence for paxilline- and NS11021-sensitive BK-mediated currents of 190 pS conductance in mitoplasts from wild-type but not BK-/- cardiomyocytes. Transmission electron microscopy of BK-/- ventricular muscles fibres showed normal ultra-structures and matrix dimension, but oxidative phosphorylation capacities at normoxia and upon re-oxygenation after anoxia were significantly attenuated in BK-/- permeabilized cardiomyocytes. In the absence of BK, post-anoxic reactive oxygen species (ROS) production from cardiomyocyte mitochondria was elevated indicating that mitoBK fine-tune the oxidative state at hypoxia and re-oxygenation. Because ROS and the capacity of the myocardium for oxidative metabolism are important determinants of cellular survival, we tested BK-/- hearts for their response in an ex-vivo model of ischemia/reperfusion (I/R) injury. Infarct areas, coronary flow and heart rates were not different between wild-type and BK-/- hearts upon I/R injury in the absence of ischemic pre-conditioning (IP), but differed upon IP. While the area of infarction comprised 28±3% of the area at risk in wild-type, it was increased to 58±5% in BK-/- hearts suggesting that BK mediates the beneficial effects of IP. These findings suggest that cardiac BK channels are important for proper oxidative energy supply of cardiomyocytes at normoxia and upon re-oxygenation after prolonged anoxia and that IP might indeed favor survival of the myocardium upon I/R injury in a BK-dependent mode stemming from both mitochondrial post-anoxic ROS modulation and non-mitochondrial localizations.
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