ArticleThe Journal of biological chemistry2010
Store-operated Ca2+ entry in malignant hyperthermia-susceptible human skeletal muscle.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 59 citations in OpenAlex.
- EMQN Best Practice Guidelines for Genetic Testing and Reporting in RYR1-related disorders.European journal of human genetics : EJHG · 2026Review
- Muscle-specific Ryanodine receptor 1 properties underlie limb-girdle muscular dystrophy 2B/R2 progression.Nature communications · 2025Article
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- Sarcoplasmic Reticulum CaCells · 2023Review
- Malignant Hyperthermia in PICU-From Diagnosis to Treatment in the Light of Up-to-Date Knowledge.Children (Basel, Switzerland) · 2022Review
- Gene Panel Sequencing Identifies a NovelGenes · 2022Article
- Store-Operated CaInternational journal of molecular sciences · 2022Article
- Altered CaMetabolites · 2021Review
- Molecular Modification of Transient Receptor Potential Canonical 6 Channels Modulates Calcium Dyshomeostasis in a Mouse Model Relevant to Malignant Hyperthermia.Anesthesiology · 2021Article
- The Orai1 inhibitor BTP2 has multiple effects on Ca2+ handling in skeletal muscle.The Journal of general physiology · 2021Article
- Enhanced Store-Operated CaFrontiers in physiology · 2021Article
- Physiological and Pathological Relevance of Selective and Nonselective CaAdvances in experimental medicine and biology · 2021Article
- Calsequestrin: a well-known but curious protein in skeletal muscle.Experimental & molecular medicine · 2020Review
- Excessive Accumulation of CaFrontiers in physiology · 2019Article
- Role of STIM1/ORAI1-mediated store-operated CaCell calcium · 2018Review
- With the greatest care, stromal interaction molecule (STIM) proteins verify what skeletal muscle is doing.BMB reports · 2018Review
- SOCE Is Important for Maintaining Sarcoplasmic Calcium Content and Release in Skeletal Muscle Fibers.Biophysical journal · 2017Article
- A focus on extracellular CaExperimental & molecular medicine · 2017Review
- Strenuous exercise triggers a life-threatening response in mice susceptible to malignant hyperthermia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Dantrolene requires MgProceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In malignant hyperthermia (MH), mutations in RyR1 underlie direct activation of the channel by volatile anesthetics, leading to muscle contracture and a life-threatening increase in core body temperature. The aim of the present study was to establish whether the associated depletion of sarcoplasmic reticulum (SR) Ca(2+) triggers sarcolemmal Ca(2+) influx via store-operated Ca(2+) entry (SOCE). Samples of vastus medialis muscle were obtained from patients undergoing assessment for MH susceptibility using the in vitro contracture test. Single fibers were mechanically skinned, and confocal microscopy was used to detect changes in [Ca(2+)] either within the resealed t-system ([Ca(2+)](t-sys)) or within the cytosol. In normal fibers, halothane (0.5 mM) failed to initiate SR Ca(2+) release or Ca(2+)(t-sys) depletion. However, in MH-susceptible (MHS) fibers, halothane induced both SR Ca(2+) release and Ca(2+)(t-sys) depletion, consistent with SOCE. In some MHS fibers, halothane-induced SR Ca(2+) release took the form of a propagated wave, which was temporally coupled to a wave of Ca(2+)(t-sys) depletion. SOCE was potently inhibited by "extracellular" application of a STIM1 antibody trapped within the t-system but not when the antibody was denatured by heating. In conclusion, (i) in human MHS muscle, SR Ca(2+) depletion induced by a level of volatile anesthetic within the clinical range is sufficient to induce SOCE, which is tightly coupled to SR Ca(2+) release; (ii) sarcolemmal STIM1 has an important role in regulating SOCE; and (iii) sustained SOCE from an effectively infinite extracellular Ca(2+) pool may contribute to the maintained rise in cytosolic [Ca(2+)] that underlies MH.
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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.