Abstract
In the heart muscle, Ca2+-induced Ca2+ release (CICR) is the main mechanism for Ca2+ increase required for the excitation-contraction coupling. However, a second mechanism for Ca2+ release from the sarcoplasmic reticulum induced by inositol 1,4,5-trisphosphate (IP3), called inositol IP3-induced intracellular Ca2+ release (IP3ICR), has been verified in cardiomyocytes. Occurrence of global Ca2+ transients as well as spontaneous Ca2+ waves (SCaW) are driven by CICR. Under pathophysiological remodeling conditions in which an up-regulation of IP3 receptors (IP3Rs) was observed, a modulatory role of IP3ICR on CICR seems plausible.
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