Atherosclerosis
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Our goal was to examine the interaction between vitamin D and statins and the possible role of vitamin D deficiency in statin myopathy. ⋯ Our review suggests that some but not all statins increase 25(OH) D levels. Two cross sectional studies have associated vitamin D deficiency with statin-associated myalgias, and suggested that that increasing vitamin D levels can reverse the myalgia. Nevertheless, given the quality and paucity of studies examining this possibility, additional studies are needed to examine the potential role of vitamin D deficiency in statin myopathy. It is presently premature to recommend vitamin D supplementation as treatment for statin associated muscle complaints in the absence of low vitamin D levels although such supplementation could be tried in patients with deficient or reduced vitamin D levels.
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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.
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Leptin is an adipocyte-derived hormone that has been shown to exert both beneficial metabolic effects and potentially adverse vascular effects in preclinical studies. The primary aim of this study was to determine the effects of leptin receptor signaling pathways on atherosclerosis in the setting of obesity and hyperlipidemia. ⋯ In a mouse model of obesity and hyperlipidemia, leptin receptor-mediated STAT3-independent signaling pathways confer protection against atherosclerosis. These differences occur independently of leptin effects on energy balance.