Ca²⁺ Release via IP₃ Receptors Shapes the Cardiac Ca²⁺ Transient for Hypertrophic Signaling.

ABSTRACT: Calcium (Ca²⁺) plays a central role in mediating both contractile function and hypertrophic signaling in ventricular cardiomyocytes. L-type Ca²⁺ channels trigger release of Ca²⁺ from ryanodine receptors for cellular contraction, whereas signaling downstream of G-protein-coupled receptors stimulates Ca²⁺ release via inositol 1,4,5-trisphosphate receptors (IP₃Rs), engaging hypertrophic signaling pathways. Modulation of the amplitude, duration, and duty cycle of the cytosolic Ca²⁺ contraction signal and spatial localization have all been proposed to encode this hypertrophic signal. Given current knowledge of IP₃Rs, we develop a model describing the effect of functional interaction (cross talk) between ryanodine recep

SUBMITTER: Hunt H 

PROVIDER: S-EPMC7499065 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature