Vitamin E and vascular homeostasis: implications for atherosclerosis.
Considerable epidemiologic data suggest that dietary consumption of vitamin E reduces the incidence of cardiovascular disease. The precise mechanisms are not clear, but emerging data indicate that vitamin E has numerous activities that may, in part, explain its effect on vascular disease. In particular, vitamin E enhances the bioactivity of nitric oxide, inhibits smooth muscle proliferation, and limits platelet aggregation. One common mechanism to account for these effects of vitamin E is the inhibition of protein kinase C stimulation. In the setting of atherosclerosis, inhibition of protein kinase C by vitamin E would be expected to maintain normal vascular homeostasis and thus reduce the clinical incidence of cardiovascular disease.
Keaney
J F
JF
Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. jkeaney@bu.edu
Simon
D I
DI
Freedman
J E
JE
D000975:Antioxidants / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000188:drug therapy / Q000209:etiology*; D001773:Blood Cells / Q000187:drug effects; D001808:Blood Vessels / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects; D006706:Homeostasis; D006801:Humans; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D014810:Vitamin E / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use
D000975:Antioxidants; D014810:Vitamin E; D009569:Nitric Oxide; D011493:Protein Kinase C