Long Term Regulation of Cardiac L-Type Calcium Channel by Small G Proteins

J.      Magyar; A.      Jenes; K.      Kistamas; F.      Ruzsnavszky; P.      P. Nanasi; J.      Satin; N.      Szentandrassy; T.      Banyasz

doi:10.2174/092986711796642436

Abstract

Calcium ions are crucial elements of excitation-contraction coupling in cardiac myocytes. The intracellular Ca2+ concentration changes continously during the cardiac cycle, but the Ca2+ entering to the cell serves as an intracellular second messenger, as well. The Ca2+ as a second messenger influences the activity of many intracellular signalling pathways and regulates gene expression. In cardiac myocytes the major pathway for Ca2+ entry into cells is L-type calcium channel (LTCC). The precise control of LTCC function is essential for maintaining the calcium homeostasis of cardiac myocytes. Dysregulation of LTCC may result in different diseases like cardiac hypertrophy, arrhytmias, heart failure. The physiological and pathological structural changes in the heart are induced in part by small G proteins. These proteins are involved in wide spectrum of cell biological functions including protein transport, regulation of cell proliferation, migration, apoptosis, and cytoskeletal rearrangement. Understanding the crosstalk between small G proteins and LTCC may help to understand the pathomechanism of different cardiac diseases and to develop a new generation of genetically-encoded Ca2+ channel inhibitors.

Keywords: Small G protein, calcium channel, heart, Calcium ions, crucial elements, excitation-contraction coupling, cardiac myocytes, intracellular Ca2+ concentration, cardiac cycle, signalling pathways