Abstract
In cardiac and skeletal muscle Ca 2+ release from intracellular stores triggers actomyosin cross-bridge formation and the generation of contractile force. In the face of large fluctuations of intracellular calcium ([Ca 2+] i ) that occur with contractile activity, myocytes are able to sense and respond to changes in workload and patterns of activation through calcium signaling pathways which modulate gene expression and cellular metabolism. Store-operated calcium influx has emerged as a mechanism by which calcium signaling pathways are activated in order to respond to the changing demands of the myocyte. Abnormalities of store-operated calcium influx may contribute to maladaptive muscle remodeling in multiple disease states. The importance of store-operated calcium influx in muscle is confirmed in mice lacking STIM1 which die perinatally and in patients with mutations on STIM1 or Orai1 who exhibit a myopathy exhibited by hypotonia. In this review, we consider the role of store-operated Ca 2+ entry into skeletal muscle as a critical mediator of Ca 2+ dependent gene expression and how alterations in Ca 2+ influx may influence muscle development and disease.
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