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Role of STIM1/ORAI1-mediated store-operated Ca2+ entry in skeletal muscle physiology and disease.
Cell Calcium. 2018 12; 76:101-115.CC

Abstract

Store-operated Ca2+ entry (SOCE) is a Ca2+ entry mechanism activated by depletion of intracellular Ca2+ stores. In skeletal muscle, SOCE is mediated by an interaction between stromal-interacting molecule-1 (STIM1), the Ca2+ sensor of the sarcoplasmic reticulum, and ORAI1, the Ca2+-release-activated-Ca2+ (CRAC) channel located in the transverse tubule membrane. This review focuses on the molecular mechanisms and physiological role of SOCE in skeletal muscle, as well as how alterations in STIM1/ORAI1-mediated SOCE contribute to muscle disease. Recent evidence indicates that SOCE plays an important role in both muscle development/growth and fatigue. The importance of SOCE in muscle is further underscored by the discovery that loss- and gain-of-function mutations in STIM1 and ORAI1 result in an eclectic array of disorders with clinical myopathy as central defining component. Despite differences in clinical phenotype, all STIM1/ORAI1 gain-of-function mutations-linked myopathies are characterized by the abnormal accumulation of intracellular membranes, known as tubular aggregates. Finally, dysfunctional STIM1/ORAI1-mediated SOCE also contributes to the pathogenesis of muscular dystrophy, malignant hyperthermia, and sarcopenia. The picture to emerge is that tight regulation of STIM1/ORAI1-dependent Ca2+ signaling is critical for optimal skeletal muscle development/function such that either aberrant increases or decreases in SOCE activity result in muscle dysfunction.

Authors+Show Affiliations

Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, 14642, United States.Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, 14642, United States.CeSI-Met - Center for Research on Ageing and Translational Medicine, and DNICS, Department of Neuroscience, Imaging and Clinical Sciences, University G. d'Annunzio, Chieti, I-66100, Italy.Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, 14642, United States. Electronic address: Robert_Dirksen@URMC.Rochester.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

30414508

Citation

Michelucci, Antonio, et al. "Role of STIM1/ORAI1-mediated Store-operated Ca2+ Entry in Skeletal Muscle Physiology and Disease." Cell Calcium, vol. 76, 2018, pp. 101-115.
Michelucci A, García-Castañeda M, Boncompagni S, et al. Role of STIM1/ORAI1-mediated store-operated Ca2+ entry in skeletal muscle physiology and disease. Cell Calcium. 2018;76:101-115.
Michelucci, A., García-Castañeda, M., Boncompagni, S., & Dirksen, R. T. (2018). Role of STIM1/ORAI1-mediated store-operated Ca2+ entry in skeletal muscle physiology and disease. Cell Calcium, 76, 101-115. https://doi.org/10.1016/j.ceca.2018.10.004
Michelucci A, et al. Role of STIM1/ORAI1-mediated Store-operated Ca2+ Entry in Skeletal Muscle Physiology and Disease. Cell Calcium. 2018;76:101-115. PubMed PMID: 30414508.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of STIM1/ORAI1-mediated store-operated Ca2+ entry in skeletal muscle physiology and disease. AU - Michelucci,Antonio, AU - García-Castañeda,Maricela, AU - Boncompagni,Simona, AU - Dirksen,Robert T, Y1 - 2018/10/30/ PY - 2018/08/06/received PY - 2018/10/23/revised PY - 2018/10/23/accepted PY - 2018/11/11/pubmed PY - 2019/8/10/medline PY - 2018/11/11/entrez KW - Ca(2+) signaling KW - Ca(2+)-release-activated-Ca(2+) (CRAC) KW - Muscle fatigue KW - Tubular aggregate myopathy (TAM) SP - 101 EP - 115 JF - Cell calcium JO - Cell Calcium VL - 76 N2 - Store-operated Ca2+ entry (SOCE) is a Ca2+ entry mechanism activated by depletion of intracellular Ca2+ stores. In skeletal muscle, SOCE is mediated by an interaction between stromal-interacting molecule-1 (STIM1), the Ca2+ sensor of the sarcoplasmic reticulum, and ORAI1, the Ca2+-release-activated-Ca2+ (CRAC) channel located in the transverse tubule membrane. This review focuses on the molecular mechanisms and physiological role of SOCE in skeletal muscle, as well as how alterations in STIM1/ORAI1-mediated SOCE contribute to muscle disease. Recent evidence indicates that SOCE plays an important role in both muscle development/growth and fatigue. The importance of SOCE in muscle is further underscored by the discovery that loss- and gain-of-function mutations in STIM1 and ORAI1 result in an eclectic array of disorders with clinical myopathy as central defining component. Despite differences in clinical phenotype, all STIM1/ORAI1 gain-of-function mutations-linked myopathies are characterized by the abnormal accumulation of intracellular membranes, known as tubular aggregates. Finally, dysfunctional STIM1/ORAI1-mediated SOCE also contributes to the pathogenesis of muscular dystrophy, malignant hyperthermia, and sarcopenia. The picture to emerge is that tight regulation of STIM1/ORAI1-dependent Ca2+ signaling is critical for optimal skeletal muscle development/function such that either aberrant increases or decreases in SOCE activity result in muscle dysfunction. SN - 1532-1991 UR - https://www.unboundmedicine.com/medline/citation/30414508/Role_of_STIM1/ORAI1_mediated_store_operated_Ca2+_entry_in_skeletal_muscle_physiology_and_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0143-4160(18)30136-2 DB - PRIME DP - Unbound Medicine ER -