Atherosclerosis
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Excessive adventitial neovascularization is one of the hallmarks of atherosclerotic plaque progression and is associated with an increased plaque burden by facilitating leukocyte influx and perivascular inflammation. Statins act atheroprotective by reducing plasma cholesterol levels and by quenching inflammation, but recent studies suggest that they may also affect neovascularization. In this study, we aimed to investigate this notion in apoE(-/-) mice. ⋯ Furthermore, endothelial proliferation was significantly inhibited by atorvastatin treatment in vitro. In conclusion, atorvastatin treatment inhibits plaque development in ApoE deficient mice independent of plasma total cholesterol levels. Given the profound inhibition of adventitial neovascularization, we propose that statins may partly exert their protective effects by modulating this process, identifying yet another atheroprotective mechanism for statins.
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Polymorphisms of the transforming growth factor-β1 (TGFB1) gene have not been associated with asymptomatic atherosclerosis previously. We investigated the relationship between a single nucleotide polymorphism (SNP) rs4803455 in TGFB1 and atherosclerosis identified by the presence of carotid plaque and increased intima-media thickness (IMT) in an older Chinese population. ⋯ This is the first study to show that the C allele in TGFB1 was associated with increased risk of atherosclerosis in older Chinese men. Further investigations on the linkage between the TGFB1 gene and progression of atherosclerosis in asymptomatic populations are warranted.