Voltage-dependent L-type calcium channel subunit alpha-1C (Caᵥ1.2) (Caᵥ1.2)

The cardiac L-type calcium channel Caᵥ1.2, primarily composed of the pore-forming alpha-1C subunit encoded by the CACNA1C gene, is a critical voltage-gated ion channel in the heart and vascular smooth muscle (UniProt Q00975). It mediates the influx of calcium ions during the plateau phase of the cardiac action potential, which is essential for excitation-contraction coupling and maintaining the heart's rhythm (PubMed: 21127204). In addition to its role in the cardiovascular system, Caᵥ1.2 is expressed in the brain, where it contributes to synaptic plasticity, learning, and memory (Frontiers in Aging Neuroscience, 2022). Mutations in the CACNA1C gene are associated with severe channelopathies, including Timothy syndrome and Long QT syndrome type 8, which can lead to life-threatening arrhythmias (PubMed: 36272554). Pharmacologically, Caᵥ1.2 is the primary target for calcium channel blockers such as dihydropyridines (e.g., nifedipine), phenylalkylamines (e.g., verapamil), and benzothiazepines (e.g., diltiazem) (StatPearls, 2023). These drugs inhibit calcium entry, leading to vasodilation and decreased cardiac contractility, making them cornerstone treatments for hypertension and angina. However, therapeutic challenges include managing side effects like hypotension and bradycardia, as well as addressing reduced drug efficacy in specific genetic variants (Journal of Molecular and Cellular Cardiology, 2022).

Other names

CACNA1CCaV1.2L-type calcium channel alpha 1C subunitCCHL1A1Calcium channel, L type, alpha 1 polypeptide, cardiac muscleVoltage-gated calcium channel alpha subunit Cav1.2

Calcium channel blockade