Abstract
Ca 2+ sparks are the fundamental units that comprise Ca 2+-induced Ca 2+ release (CICR) in striated muscle cells. In cardiac muscle, spontaneous Ca 2+ sparks underlie the rhythmic CICR activity during heart contraction. In skeletal muscle, Ca 2+ sparks remain quiescent during the resting state and are activated in a plastic fashion to accommodate various levels of stress. With aging, the plastic Ca 2+ spark signal becomes static in skeletal muscle, whereas loss of CICR control leads to leaky Ca 2+ spark activity in aged cardiomyocytes. Ca 2+ spark responses reflect the integrated function of the intracellular Ca 2+ regulatory machinery centered around the triad or dyad junctional complexes of striated muscles, which harbor the principal molecular players of excitation–contraction coupling. This review highlights the contribution of age-related modification of the Ca 2+ release machinery and the effect of membrane structure and membrane cross-talk on the altered Ca 2+ spark signaling during aging of striated muscles.
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Published Version
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