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Intracellular Ca 2+ ions represent a signaling mediator that plays a critical role in regulating different muscular cellular processes. Ca 2+ homeostasis preservation is essential for maintaining skeletal muscle structure and function. Store-operated Ca 2+ entry (SOCE), a Ca 2+ -entry process activated by depletion of intracellular stores contributing to the regulation of various function in many cell types, is pivotal to ensure a proper Ca 2+ homeostasis in muscle fibers. It is coordinated by STIM1, the main Ca 2+ sensor located in the sarcoplasmic reticulum, and ORAI1 protein, a Ca 2+ -permeable channel located on transverse tubules. It is commonly accepted that Ca 2+ entry via SOCE has the crucial role in short- and long-term muscle function, regulating and adapting many cellular processes including muscle contractility, postnatal development, myofiber phenotype and plasticity. Lack or mutations of STIM1 and/or Orai1 and the consequent SOCE alteration have been associated with serious consequences for muscle function. Importantly, evidence suggests that SOCE alteration can trigger a change of intracellular Ca 2+ signaling in skeletal muscle, participating in the pathogenesis of different progressive muscle diseases such as tubular aggregate myopathy, muscular dystrophy, cachexia, and sarcopenia. This review provides a brief overview of the molecular mechanisms underlying STIM1/Orai1-dependent SOCE in skeletal muscle, focusing on how SOCE alteration could contribute to skeletal muscle wasting disorders and on how SOCE components could represent pharmacological targets with high therapeutic potential.

Alteration of STIM1/Orai1-Mediated SOCE in Skeletal Muscle: Impact in Genetic Muscle Diseases and Beyond