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Cigarette-induced endothelial dysfunction could be an early mediator of atherosclerosis. In this study, we explored the mechanisms of cigarette smoke extract (CSE)-induced human aortic endothelial cells (HAEC) apoptosis. We found that 10–65% of HAECs underwent apoptotic changes when HAECs were exposed to 0.001–0.02 cigarette equivalent unit of CSE for 4h. CSE activated the caspases-3 and 8, the p38...
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