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Background Multiple evidences indicated that statins exhibit atheroprotective effects greater than those anticipated from LDL-lowering alone.Rosuvastatin has been reported to increase anticoagulants and decrease procoagulants in human umbilical vein endothelial cells (HUVECs).KLF2 was strongly implicated to be a novel nuclear mediator of statin effects in endothelial cells.We hypothesized that rosuvastatin might induce the expression and activity of KLF2 in order to protect thrombosis.