Hepatic stellate cells (HSCs) are largely involved in hepatic fibrosis associated with liver diseases such as non-alcoholic steatohepatitis. An increase in cytosolic [Ca²⁺] in HSCs facilitates hepatic fibrosis, however, the regulatory mechanism is unclear. T-type voltage-dependent Ca²⁺ channels (T-VDCCs) contribute to neuronal transmission and cardiac rhythm in excitable cells. Recently, the pathophysiological roles of T-VDCCs in non-excitable cells such as cancer cells and immune cells have been focused. Under whole-cell patch-clamp configurations, transient inward currents were observed in mouse activated HSCs, but not in quiescent HSCs. Quantitative real-time PCR analysis revealed that the mRNA expression of T-VDCCs was significantly higher in activated HSCs than in quiescent HSCs. The viability of activated HSCs was significantly reduced by the treatment with T-VDCC inhibitors. These results suggest that the upregulation of T-VDCC expression in activated HSCs contributes to the regulation of Ca²⁺ signaling and cell proliferation. This study may contribute to the comprehensive understanding of HSC functions in hepatic fibrosis.