Key result
Calcium and IP3 signaling exhibit non-linear coordination to regulate levels in cardiac myocytes.
Why the study?
Abnormalities in calcium signaling are implicated in heart failure and arrhythmias, but the complex interdependent dynamics of calcium and IP3 in cardiac myocytes require systematic investigation.
Mathematical model of Ca2+/IP3 signaling may guide arrhythmia hypotheses; leaves open validation before any clinical use.
Calcium (Ca 2+ ) and inositol 1,4,5-trisphosphate (IP 3 ) is critically important actors for a vast array of cellular processes. The most significant of the functions is One of the main functions is communication in all parts of the body which is achieved through cell signaling. Abnormalities in Ca 2+ signaling have been implicated in clinically important conditions such as heart failure and cardiac arrhythmias. We propose a mathematical model which systematically investigates complex Ca 2+ and IP 3 dynamics in cardiac myocyte. This two dimensional model is based on calcium-induced calcium release via inositol 1,4,5-trisphosphate receptors and includes calcium modulation of IP 3 levels through feedback regulation of degradation and production. Forward-Time Centered-Space method has been used to solve the coupled equations. We were able to reproduce the observed oscillatory patterns in Ca 2+ as well as IP 3 signals. The model predicts that calcium-dependent production and degradation of IP 3 is a key mechanism for complex calcium oscillations in cardiac myocyte. The impact and sensitivity of source, leak, diffusion coefficients on both Ca 2+ and IP 3 dynamics have been investigated. The results show that the relationship between Ca 2+ and IP 3 dynamics is nonlinear.
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Singh et al. (2019) studied Cardiac myocyte calcium signaling. Mathematical modeling of Ca2+ and IP3 dynamics was evaluated on Ca2+ and IP3 concentration dynamics. A two-dimensional mathematical model demonstrated that calcium and IP3 signaling processes are non-linearly interdependent and exhibit coordination in regulating their levels in cardiac myocytes.
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