Cav1.2 calcium channels are the principal proteins involved in electrical, mechanical, and/or signaling functions of the cell. Cav1.2 couples membrane depolarization to the transient increase in intracellular Ca(2+) concentration that is a trigger for muscle contraction and CREB-dependent transcriptional activation. The CACNA1C gene coding for the Cav1.2 pore-forming α 1C subunit is subject to extensive alternative splicing. This review is the first attempt to follow the association between cell proliferation, Cav1.2 expression and splice variation, and atherosclerosis. Based on insights into the association between the atherosclerosis-induced molecular remodeling of Cav1.2, 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.
Keyphrases
- cell proliferation
- cardiovascular disease
- vascular smooth muscle cells
- gene therapy
- single cell
- transcription factor
- angiotensin ii
- pi k akt
- copy number
- oxidative stress
- heat shock
- genome wide
- single molecule
- binding protein
- blood brain barrier
- long non coding rna
- dna methylation
- heat stress
- genome wide identification
- mesenchymal stem cells
- climate change
- genome wide analysis
- subarachnoid hemorrhage