Voltage-dependent L-type calcium channel subunit alpha-1C (CACNA1C) and Voltage-dependent L-type calcium channel subunit alpha-1D (CACNA1D) (Common abbreviations are CACNA1C (for alpha-1C) and CACNA1D (for alpha-1D). CaV1.2 (CACNA1C) and CaV1.3 (CACNA1D) are also widely used.)

Voltage-dependent L-type calcium channel subunits alpha-1C and alpha-1D are the primary pore-forming components of L-type calcium channels, crucial for calcium entry into excitable cells such as cardiac, skeletal, and smooth muscle, as well as neuronal cells[1][3][5][6]. These channels mediate influx of Ca2+ ions upon membrane depolarization, triggering essential processes like muscle contraction, pacemaker activity, hormone secretion, and signal transduction. The alpha-1C subunit (CACNA1C, CaV1.2) is especially vital in the heart where it regulates excitation-contraction coupling and cardiac rhythm, while the alpha-1D subunit (CACNA1D, CaV1.3) plays prominent roles in the endocrine system, the central nervous system, and also contributes to cardiac and muscular functions. Both are prominent drug targets for cardiovascular and neurological therapeutics, but their inhibition can evoke notable side effects due to their central physiological roles[1][3][5][6][7].

Other names

L-type calcium channel alpha-1C subunitCaV1.2CACNA1CL-type calcium channel alpha-1D subunitCaV1.3CACNA1D

Drugs such as calcium channel blockers antagonize these channels, reducing calcium influx into cardiac and smooth muscle cells, leading to decreased muscle contraction, reduced heart rate, and lowered blood pressure.