ArticleThe Journal of biological chemistry2014
Ca2+ influx via the Na+/Ca2+ exchanger is enhanced in malignant hyperthermia skeletal muscle.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Mitochondrial bioenergetics and intracellular calcium concentration in primary myotubes from mouse models of malignant hyperthermia.British journal of anaesthesia · 2026Article
- Aberrant extracellular dopamine clearance in the prefrontal cortex exhibits ADHD-like behavior in NCX3 heterozygous mice.The FEBS journal · 2025Article
- Short-Term Mild Hypoxia Modulates Na,K-ATPase to Maintain Membrane Electrogenesis in Rat Skeletal Muscle.International journal of molecular sciences · 2022Article
- Chronic Elevation of Skeletal Muscle [CaFrontiers in physiology · 2022Article
- Molecular Modification of Transient Receptor Potential Canonical 6 Channels Modulates Calcium Dyshomeostasis in a Mouse Model Relevant to Malignant Hyperthermia.Anesthesiology · 2021Article
- Physiological and Pathological Relevance of Selective and Nonselective CaAdvances in experimental medicine and biology · 2021Article
- Transient Receptor Potential Cation Channels and Calcium Dyshomeostasis in a Mouse Model Relevant to Malignant Hyperthermia.Anesthesiology · 2020Article
- Skeletal Muscle Na,K-ATPase as a Target for Circulating Ouabain.International journal of molecular sciences · 2020Article
- Senescence Is Associated With Elevated Intracellular Resting [CaFrontiers in physiology · 2020Article
- In vitro effects of levosimendan on muscle of malignant hyperthermia susceptible and non-susceptible swine.BMC anesthesiology · 2018Article
- Malignant hyperthermia, environmental heat stress, and intracellular calcium dysregulation in a mouse model expressing the p.G2435R variant of RYR1.British journal of anaesthesia · 2018Article
- Junctional membrane CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Functional and structural characterization of a novel malignant hyperthermia-susceptible variant of DHPR-βAmerican journal of physiology. Cell physiology · 2018Article
- The relationship between form and function throughout the history of excitation-contraction coupling.The Journal of general physiology · 2018Review
- Pyrethroid Insecticides Directly Activate Microglia Through Interaction With Voltage-Gated Sodium Channels.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Clinical treatment of malignant hyperthermia in three cases.Experimental and therapeutic medicine · 2016Article
- Pivotal role of α2 NaThe Journal of physiology · 2016Review
- Skeletal Muscle Microalterations in Patients Carrying Malignant Hyperthermia-Related Mutations of the e-c Coupling Machinery.European journal of translational myology · 2016Article
- Chronic heart failure: Ca(2+), catabolism, and catastrophic cell death.Biochimica et biophysica acta · 2016Review
- Hydrophobic bile acids relax rat detrusor contraction via inhibiting the opening of the Na⁺/Ca²⁺ exchanger.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Malignant hyperthermia (MH) is potentially fatal pharmacogenetic disorder of skeletal muscle caused by intracellular Ca(2+) dysregulation. NCX is a bidirectional transporter that effluxes (forward mode) or influxes (reverse mode) Ca(2+) depending on cellular activity. Resting intracellular calcium ([Ca(2+)]r) and sodium ([Na(+)]r) concentrations are elevated in MH susceptible (MHS) swine and murine muscles compared with their normal (MHN) counterparts, although the contribution of NCX is unclear. Lowering [Na(+)]e elevates [Ca(2+)]r in both MHN and MHS swine muscle fibers and it is prevented by removal of extracellular Ca(2+) or reduced by t-tubule disruption, in both genotypes. KB-R7943, a nonselective NCX3 blocker, reduced [Ca(2+)]r in both swine and murine MHN and MHS muscle fibers at rest and decreased the magnitude of the elevation of [Ca(2+)]r observed in MHS fibers after exposure to halothane. YM-244769, a high affinity reverse mode NCX3 blocker, reduces [Ca(2+)]r in MHS muscle fibers and decreases the amplitude of [Ca(2+)]r rise triggered by halothane, but had no effect on [Ca(2+)]r in MHN muscle. In addition, YM-244769 reduced the peak and area under the curve of the Ca(2+) transient elicited by high [K(+)]e and increased its rate of decay in MHS muscle fibers. siRNA knockdown of NCX3 in MHS myotubes reduced [Ca(2+)]r and the Ca(2+) transient area induced by high [K(+)]e. These results demonstrate a functional NCX3 in skeletal muscle whose activity is enhanced in MHS. Moreover reverse mode NCX3 contributes to the Ca(2+) transients associated with K(+)-induced depolarization and the halothane-triggered MH episode in MHS muscle fibers.
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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.