{"__content__"=>"\n Graphical Abstract\n \n ", "p"=>[{"__content__"=>"Activation of hepatic stellate cells (HSCs) is a pivotal event in the development of liver fibrosis, a pathological process that precedes cirrhosis and hepatocellular carcinoma and for which effective therapies remain limited. The molecular mechanisms underlying HSC activation, particularly the ion channels that regulate cytosolic Ca²⁺ signaling that promote fibrogenesis, remain incompletely understood. In this study, the expression and functional roles of Ca²⁺ channels in human and mouse HSCs were investigated using quantitative real-time PCR, Western blotting, whole-cell patch-clamp electrophysiology, Ca imaging, and histological analyses. RNA sequencing of human HSCs revealed upregulation of Ca3.2 transcripts upon activation. In activated human HSCs (LX-2 cells), Ca3.2 protein was detected, and transient inward currents sensitive to the T-type voltage-dependent Ca²⁺ channel (T-VDCC) blocker Z944 were recorded. Z944 concentration-dependently reduced both resting cytosolic Ca concentration ([Ca]) and mRNA levels of activation markers ( and ) in LX-2 cells. In mouse HSCs, Ca3.1 and Ca3.2 mRNA and protein expression increased during activation and were accompanied by Z944-sensitive inward currents. Among T-VDCC isoforms, Ca3.2 was identified as the predominant contributor to both T-type Ca²⁺ currents and resting [Ca]. In a mouse model of metabolic dysfunction-associated steatohepatitis (MASH), Ca3.2 expression was selectively elevated in HSCs. Notably, administration of Z944 significantly attenuated MASH-associated liver fibrosis compared with controls. Collectively, these findings demonstrate that Ca3.2 expression and activity are upregulated during HSC activation, resulting in enhanced cytosolic Ca²⁺ signaling and fibrogenic responses. Ca3.2 may therefore represent a potential therapeutic target for liver fibrosis.", "sup"=>[{"__content__"=>"2+"}, {"__content__"=>"2+"}, {"__content__"=>"2+"}, {"__content__"=>"2+"}], "sub"=>[{"__content__"=>"V"}, {"__content__"=>"V"}, {"__content__"=>"cyt"}, {"__content__"=>"V"}, {"__content__"=>"V"}, {"__content__"=>"V"}, {"__content__"=>"cyt"}, {"__content__"=>"V"}, {"__content__"=>"V"}, {"__content__"=>"V"}], "i"=>[{"__content__"=>"ACTA2"}, {"__content__"=>"COL3A1"}]}, {}]}