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Vitamin E and vascular homeostasis: implications for atherosclerosis
Author(s) -
Keaney John F.,
Simon Daniel I.,
Freedman Jane E.
Publication year - 1999
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.13.9.965
Subject(s) - vascular smooth muscle , vitamin d and neurology , homeostasis , medicine , endocrinology , nitric oxide , vitamin , biology , smooth muscle
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., Jr., Simon, D. I., Freedman, J. E. Vitamin E and vascular homeostasis: implications for atherosclerosis. FASEB J. 13, 965–976 (1999)
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