Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 7, Issue 2, Pages 225-232Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2006.09.010
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Ryanodine receptors RyRs) function as intracellular Ca2+ release channels on the endoplasmic and sarcoplasmic reticulum membranes. In striated muscles, Ca2+ release through RyRs controls muscle excitation-contraction coupling. RyR channel function is regulated by a cytoplasmic scaffold domain that forms a macromolecular signaling complex including calstabin (formerly known as FK506-binding protein), calmodulin, phosphodiesterase, kinase and phosphatase proteins. An increasing number of genetic and acquired diseases has been associated with intracellular Ca2+ leak. In heart failure, for instance, the RyR complex becomes altered, resulting in chronic channel dysfunction and chronic sarcoplasmic reticulum Ca2+ leak. Recently, the efficacy of novel Ca2+ release channel-stabilizing drugs has been demonstrated in cardiac and skeletal muscle disease models.
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