Volume 2013 (2013), Article ID 463527, 13 pages
1.2, Cell Proliferation, and New Target in Atherosclerosis
Humgenex, Inc., Kensington, MD 20895, USA
Received 25 February 2013; Accepted 20 March 2013
Academic Editors: I. de la Serna and H. Yonekawa
Copyright © 2013 Nikolai M. Soldatov. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1.2 calcium channels are the principal proteins involved in electrical, mechanical, and/or signaling functions of the cell. 1.2 couples membrane depolarization to the transient increase in intracellular Ca2+ concentration that is a trigger for muscle contraction and CREB-dependent transcriptional activation. The CACNA1C gene coding for the 1.2 pore-forming subunit is subject to extensive alternative splicing. This review is the first attempt to follow the association between cell proliferation, 1.2 expression and splice variation, and atherosclerosis. Based on insights into the association between the atherosclerosis-induced molecular remodeling of 1.2, proliferation of vascular smooth muscle cells, and CREB-dependent transcriptional signaling, this review will give a perspective outlook for the use of the CACNA1C exon skipping as a new potential gene therapy approach to atherosclerosis.