Atherosclerosis and
related cardiovascular diseases (CVD) represent the greatest threats to
human health worldwide. Selenium, an essential trace element, is
incorporated into selenoproteins that play crucial role on human health
and disease. Although findings from a limited number of randomized
trials have been inconsistent and can not support a protective role of
Se supplementation in CVD, 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 CVD 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 baseline
selenium status, the dose and forms of selenium supplementation, and
selenoprotein genotype. Additionally, much more studies are needed to
confirm the roles of selenoproteins in atherosclerosis prevention and
clarify the underlying mechanisms.
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