Selenium in the prevention of atherosclerosis and its underlying mechanisms

Abstract

Atherosclerosis and related cardiovascular diseases (CVDs) represent the greatest threats to human health worldwide. Selenium, an essential trace element, is incorporated into selenoproteins that play a crucial role in human health and disease. Although findings from a limited number of randomized trials have been inconsistent and cannot support a protective role of Se supplementation in CVDs, prospective observational studies have generally shown a significant inverse association between selenium or selenoprotein status and CVD risk. Furthermore, a benefit of selenium supplementation in the prevention of CVDs has been seen in population with low baseline selenium status. Evidence from animal studies shows consistent results that selenium and selenoproteins might prevent experimental atherosclerosis, which can be explained by the molecular and cellular effects of selenium observed both in animal models and cell cultures. Selenoproteins of particular relevance to atherosclerosis are glutathione peroxidases, thioredoxin reductase 1, selenoprotein P, selenoprotein S. The present review is focusing on the existing evidence that supports the concept that optimal selenium intake can prevent atherosclerosis. Its underlying mechanisms include inhibiting oxidative stress, modulating inflammation, suppressing endothelial dysfunction, and protecting vascular cells against apoptosis and calcification. However, the benefit of selenium supplementation in the prevention of atherosclerosis remains insufficiently documented so far. Future studies with regard to the effects of selenium supplementation on atherosclerosis should consider many factors, especially the baseline selenium status, the dose and forms of selenium supplementation, and the selenoprotein genotype. Additionally, much more studies are needed to confirm the roles of selenoproteins in atherosclerosis prevention and clarify the underlying mechanisms.