@entity731 formation and progression are dependent on local shear stress patterns and inflammatory cytokines. Statins effectively reduce the progression of @entity731 and the incidence of @entity65 . However, the benefit of statins cannot be explained by @entity165 reduction alone. This study, investigated the non-lipid lowering effects of @entity3413 and @entity8671 on endothelial anti- and prothrombotic genes under different biomechanical and inflammatory stress conditions. Endothelial cells responded in a similar way to @entity3413 and @entity8671 . However, they were more sensitive to @entity3413 . The statins had anti-inflammatory properties counteracting the @entity310 effect on the hemostatic genes studied. There was no observed synergistic effect between shear stress and @entity3413 . @entity3413 had a counteracting effect on @entity3479 and @entity2289 compared to @entity310 and shear stress. @entity3413 blocked the @entity310 suppressive effect on thrombomodulin and eNOS, irrespective of shear stress. The strong inductive effect of @entity310 on @entity4725 was counteracted by @entity3413 and shear stress in an additive dose-response dependent way.

Effect of shear stress, statins and XXXX on hemostatic genes in human endothelial cells.

@entity2289 :: ('5054', 'Gene') :: ['PAI-1'] @entity3413 :: ('MESH:D019821', 'Chemical') :: ['Simvastatin', 'simvastatin'] @entity310 :: ('7124', 'Gene') :: ['TNF-a'] @entity8671 :: ('MESH:C422923', 'Chemical') :: ['rosuvastatin'] @entity4725 :: ('7412', 'Gene') :: ['VCAM-1'] @entity731 :: ('MESH:D050197', 'Disease') :: ['atherosclerosis', 'Atherosclerotic plaque'] @entity3479 :: ('5327', 'Gene') :: ['t-PA'] @entity65 :: ('MESH:D002318', 'Disease') :: ['cardiovascular events'] @entity165 :: ('MESH:D002784', 'Chemical') :: ['cholesterol']
@entity310 :: (7124,Gene) :: ['TNF-a']
