Cellular, molecular and clinical aspects of vitamin E on atherosclerosis prevention.
Randomised clinical trials and epidemiologic studies addressing the preventive effects of vitamin E supplementation against cardiovascular disease reported both positive and negative effects, and recent meta-analyses of the clinical studies were rather disappointing. In contrast to that, many animal studies clearly show a preventive action of vitamin E in several experimental settings, which can be explained by the molecular and cellular effects of vitamin E observed in cell cultures. This review is focusing on the molecular effects of vitamin E on the cells playing a role during atherosclerosis, in particular on the endothelial cells, vascular smooth muscle cells, monocytes/macrophages, T cells, and mast cells. Vitamin E may act by normalizing aberrant signal transduction and gene expression in antioxidant and non-antioxidant manners; in particular, over-expression of scavenger receptors and consequent foam cell formation can be prevented by vitamin E. In addition to that, the cellular effects of alpha-tocopheryl phosphate and of EPC-K1, a composite molecule between alpha-tocopheryl phosphate and l-ascorbic acid, are summarized.
Munteanu
Adelina
A
Physiology Department, Faculty of Medicine, University of Medicine and Pharmacy Bucharest, Romania.
Zingg
Jean-Marc
JM
D000818:Animals; D050197:Atherosclerosis / Q000473:pathology / Q000517:prevention & control*; D001808:Blood Vessels / Q000473:pathology; D005786:Gene Expression Regulation; D006801:Humans; D015398:Signal Transduction; D014810:Vitamin E / Q000378:metabolism*