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Abstract
Alterations in lipid profiles have been shown in patients with COPD, but the underlying molecular mechanisms remain unclear. In this study, we aim to investigate the role of CYP1B1 in cigarette smoke (CS)-induced lipid accumulation in alveolar type II epithelial (AT2) cells. We observed an increase in CYP1B1 protein levels in AT2 cells from COPD patients. CS exposure induced CYP1B1 expression in AT2 cells. Treatment with cigarette smoke extract upregulated CYP1B1 expression and triggered lipid accumulation in AT2 cells. siRNA-mediated CYP1B1 inhibition reduced CSE-induced lipid accumulation in cells. EVE exposure also induced lipid accumulation, suppressed by CYP1B1 knockdown. TMS, a selective CYP1B1 inhibitor, reduced CSE-induced lipid accumulation. TMS also attenuated CSE-induced mitochondrial reactive oxygen species (ROS) production and cell apoptosis. Our findings suggest that CYP1B1 is upregulated by CS exposure and plays a key role in CS-induced lipid accumulation in AT2 cells. Targeting CYP1B1 may offer a potential therapeutic strategy.