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Pathophysiological Role of Trpv1 In Malignant Hyperthermia: Identification of New Variants

Volume 12 - Issue 1

Nolwenn Tessier1#, Mallory Ducrozet1#, Sylvie Ducreux1, Julien Faure*2 and Fabien Van Coppenolle*1

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    • 1CarMeN laboratory, France
    • 2Laboratory of Genetic and Molecular Biochemistry, France
    • #These authors contributed equally to this work
    • #These authors jointly supervised this work
    • *Corresponding author: Fabien Van Coppenolle, France

      Julien Faure, Laboratory of Genetic and Molecular Biochemistry, France

Received: November 24, 2018;   Published: December 11, 2018

DOI: 10.26717/BJSTR.2018.12.002181

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Malignant hyperthermia is a pharmacogenetic disorder caused by volatile anesthetics that trigger severe muscle contraction and a hypermetabolic state. Outside triggered crisis, patients are asymptomatic. The molecular mechanisms of MH involve an uncontrolled increase of cytosolic Ca2+ concentration in skeletal muscles, which contributes to excessive muscle contraction and rigidity, increased body temperature, severe rhabdomyolysis and a generalized acidosis and hypermetabolic state. Mutations altering the function of the 2 main calcium channels involved in muscle contraction were so far linked to Malignant Hyperthermia. Recently, we showed that mutations in the Transient Receptor Potential Vanilloid 1 (TRPV1) cation channel could also be involved in MH. We propose that TRPV1, acting as a Ca2+ leak channel, is a target of volatile anesthetics such as isoflurane as well as a mechanism that could explain its implication in MH.

Abbreviations : MH: Malignant Hyperthermia; TRPV1: Transient Receptor Potential Vanilloid 1; RyR1: Ryanodine Receptor type 1; Ca2+: Calcium

Introduction| Conclusion| Acknowledgment| References|