Calcium signaling in cardiac myocytes

• Published in: Cold Spring Harbor perspectives in biology 2011-11, Vol.3 (11), p.a004242-a004242
• Main Authors: Fearnley, Claire J, Roderick, H Llewelyn, Bootman, Martin D
• Format: Article
• Language: English
• Subjects: Animals; Calcium - chemistry; Calcium - metabolism; Calcium Channels - physiology; Calcium Signaling; Mammals - physiology; Myocytes, Cardiac - chemistry; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - physiology; Ryanodine Receptor Calcium Release Channel - metabolism; Ryanodine Receptor Calcium Release Channel - physiology
• ISSN: 1943-0264; 1943-0264
• DOI: 10.1101/cshperspect.a004242

Calcium (Ca(2+)) is a critical regulator of cardiac myocyte function. Principally, Ca(2+) is the link between the electrical signals that pervade the heart and contraction of the myocytes to propel blood. In addition, Ca(2+) controls numerous other myocyte activities, including gene transcription. Cardiac Ca(2+) signaling essentially relies on a few critical molecular players--ryanodine receptors, voltage-operated Ca(2+) channels, and Ca(2+) pumps/transporters. These moieties are responsible for generating Ca(2+) signals upon cellular depolarization, recovery of Ca(2+) signals following cellular contraction, and setting basal conditions. Whereas these are the central players underlying cardiac Ca(2+) fluxes, networks of signaling mechanisms and accessory proteins impart complex regulation on cardiac Ca(2+) signals. Subtle changes in components of the cardiac Ca(2+) 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 Ca(2+) signaling in ventricular and atrial myocytes. In particular, we describe the roles and regulation of key participants involved in Ca(2+) signal generation and reversal.