The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Antioxidants and Atherosclerotic Heart Disease
Abstract
Epidemiologic studies have provided evidence of an inverse relation between coronary artery disease and antioxidant intake, and vitamin E supplementation in particular. The oxidative-modification hypothesis implies that reduced atherosclerosis is a result of the production of LDL that is resistant to oxidation, but linking the reduced oxidation of LDL to a reduction in atherosclerosis has been problematic. Several important additional mechanisms may underlie the role of antioxidants in preventing the clinical manifestations of coronary artery disease (Fig. 2). Specifically, there is evidence that plaque stability, vasomotor function, and the tendency to thrombosis are subject to modification by specific antioxidants. For example, cellular antioxidants inhibit monocyte adhesion, protect against the cytotoxic effects of oxidized LDL, and inhibit platelet activation. Furthermore, cellular antioxidants protect against the endothelial dysfunction associated with atherosclerosis by preserving endothelium-derived nitric oxide activity. We speculate that these mechanisms have an important role in the benefits of antioxidants.
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Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis
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Close Relation of Endothelial Function in the Human Coronary and Peripheral Circulations
Anderson, T. J., Uehata, A., Gerhard, M. D., Meredith, I. T., Knab, S., Delagrange, D., Lieberman, E. H., Ganz, P., Creager, M. A., Yeung, A. C., et al. (1995) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(95)00327-4 · Cited by 2,033
Hypercholesterolemia increases endothelial superoxide anion production.
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Ascorbic Acid Reverses Endothelial Vasomotor Dysfunction in Patients With Coronary Artery Disease
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Self-citationProbucol and Multivitamins in the Prevention of Restenosis after Coronary Angioplasty
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Self-citationWalldius, G., Erikson, U., Olsson, A. G., Bergstrand, L., Hådell, K., Johansson, J., Kaijser, L., Lassvik, C., Mölgaard, J., Nilsson, S., et al. (1994) · The American Journal of Cardiology · doi:10.1016/0002-9149(94)90579-7 · Cited by 248
Cited by
Atherosclerosis--an inflammatory disease
Ross, R. (1999) · New England Journal of Medicine · doi:10.1056/nejm199901143400207 · Cited by 21,725
Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes
Evans, J. L., Goldfine, I. D., Maddux, B. A., & Grodsky, G. M. (2002) · Endocrine Reviews · doi:10.1210/er.2001-0039 · Cited by 2,232
Kurutas, E. B. (2015) · Nutrition Journal · doi:10.1186/s12937-016-0186-5 · Cited by 2,152
The clinical implications of endothelial dysfunction
Widlansky, M. E., Gokce, N., Keaney, J. F., & Vita, J. A. (2003) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(03)00994-x · Cited by 1,749
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Metadata
- Authors
- Diaz, M. N., Frei, B., Vita, J. A., & Keaney, J. F.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1997-08-07
- Volume
- 337
- Issue
- 6
- Pages
- 408-416
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2313837936
- Cited by
- 1,353
- References
- 10
- FWCI
- 59.52
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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