The ubiquitous intracellular second messenger Ca2+ is an integral part of several signalling pathways controlling different phases of the cell cycle. Accordingly, cell proliferation has been suggested to depend on increases in intracellular Ca2+. In many cell types, Ca2+ levels can be effectively controlled via regulation of transmembrane Ca2+ influx through voltage-gated calcium channels (Cav channels). In the present study, we tested the hypothesis whether Ca2+ influx through Cav channels is involved in the regulation of human lens epithelial cell proliferation (HLEC). Proliferation of HLECs in cell culture was studied under control conditions and in the presence of the L- and T-type Cav channel blockers Mibefradil (T-type) and Verapamil (L-type). Both Cav channel blockers reduced HLEC proliferation, as well as the activation of c-Raf, MAPK 3 and CaMKII. The use of MnCl2 on Fura-2-loaded cells to determine the kinetics of Ca2+ influx (quenching technique) revealed a reduction of the fluorescence signal after 1min to 57±3% (n=3) under control conditions. This reduction was less in the presence of 10 mM Mibefradil (to 67±2%, n=3) or Verapamil (to 62±2%, n=3). We conclude that the transmembrane influx of Ca2+ through Cav channels contributes to the regulation of HLEC proliferation, identifying Cav channel blockers as potential therapeutic substances in ocular diseases.