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Abstract
Contraction is a central feature for skeletal, cardiac and smooth muscle; this unique
feature is largely dependent on calcium (Ca 2+ ) signaling and therefore maintenance
of internal Ca 2+ stores. Stromal interaction molecule 1 (STIM1) is a single-pass
transmembrane protein that functions as a Ca 2+ sensor for the activation store-operated
calcium channels (SOCCs) on the plasma membrane in response to depleted internal sarco(endo)plasmic
(S/ER) reticulum Ca 2+ stores. STIM1 was initially characterized in nonexcitable
cells; however, evidence from both animal models and human mutations suggests a role
for STIM1 in modulating Ca 2+ homeostasis in excitable tissues as well. STIM1-dependent
SOCE is particularly important in tissues undergoing sustained contraction, leading
us to believe STIM1 may play a role in smooth muscle contraction. To date, the role
of STIM1 in smooth muscle is unknown. In this review, we provide a brief overview
of the role of STIM1-dependent SOCE in striated muscle and build off that knowledge
to investigate whether STIM1 contributes to smooth muscle contractility. We conclude
by discussing the translational implications of targeting STIM1 in the treatment of
smooth muscle disorders.