Calcium Signaling in Cardiac Myocytes

Calcium (Ca2+) is a critical regulator of cardiac myocyte function. Principally, Ca2+ is the link between the electrical signals that pervade the heart and contraction of the myocytes to propel blood. In addition, Ca2+ controls numerous other myocyte activities, including gene transcription. Cardiac Ca2+ signaling essentially relies on a few critical molecular players-ryanodine receptors, voltage-operated Ca2+ channels, and Ca2+ pumps/transporters. These moieties are responsible for generating Ca2+ signals upon cellular depolarization, recovery of Ca2+ signals following cellular contraction, and setting basal conditions. Whereas these are the central players underlying cardiac Ca2+ fluxes, networks of signaling mechanisms and accessory proteins impart complex regulation on cardiac Ca2+ signals. Subtle changes in components of the cardiac Ca2+ signaling machinery, albeit through mutation, disease, or chronic alteration of hemodynamic demand, can have profound consequences for the function and phenotype of myocytes. Here, we discuss mechanisms underlying Ca2+ signaling in ventricular and atrial myocytes. In particular, we describe the roles and regulation of key participants involved in Ca2+ signal generation and reversal.