Modeling IP₃-Dependent Calcium Dynamics in Non-Excitable Cells

Abstract

Calcium is critically important for a vast array of cellular functions, as discussed in detail in Chap. 1. There are a number of Ca²⁺ control mechanisms operating on different levels, all designed to ensure that Ca²⁺ is present in sufficient quantity to perform its necessary functions, but not in too great a quantity in the wrong places. Prolonged high concentrations of Ca²⁺ are toxic. For instance, it is known that cellular Ca²⁺ overload can trigger apoptotic cell death, a process in which the cell kills itself. Indeed, control of Ca²⁺ homeostasis is so crucial that even just disruptions in the normal Ca²⁺ fluxes can lead to initiation of active cell death. There are many reviews of Ca²⁺ physiology in the literature: in 2003 an entire issue of Nature Reviews was devoted to the subject and contains reviews of Ca²⁺ homeostasis (Berridge et al., 2003), extracellular Ca²⁺ sensing (Hofer and Brown, 2003), Ca²⁺ signaling during embryogenesis (Webb and Miller, 2003), the Ca²⁺-apoptosis link (Orrenius et al., 2003), and the regulation of cardiac contractility by Ca²⁺ (MacLennan and Kranias, 2003). Other useful reviews are Berridge, (1997) and Carafoli (2002).