The role of vitamin E in atherogenesis: linking the chemical, biological and clinical aspects of the disease

• Published in: Atherosclerosis Vol. 157; no. 2; pp. 257 - 283
• Main Authors: Neuzil, Jiri, Weber, Christian, Kontush, Anatol
• Format: Book Review Journal Article
• Language: English
• Published: Amsterdam Elsevier Ireland Ltd 01.08.2001; Elsevier
• Subjects: Animals; Arteriosclerosis - etiology; Atherogenesis; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Disease Progression; Epidemiology; Humans; Immune system; Immune System - physiology; LDL modification; Medical sciences; Oxidation; Oxidation-Reduction; Signal Transduction - physiology; Signalling; Supplementation; Vascular biology; Vitamin E; Vitamin E - physiology; Atherogenesis; TNFα, tumour necrosis factor-α; ICAM1, intercellular adhesion molecule-1; Epidemiology; MI, myocardial infarction; Vitamin E; TMP, tocopherol-mediated peroxidation; apoE, apolipoprotein E; oxLDL, oxidised LDL; Oxidation; IU, international unit(s); VCAM1, vascular cell adhesion molecule-1; Supplementation; LDL, low-density lipoprotein; LO, (15-)lipoxygenase; Immune system; NFκB, nuclear factor κB; SMC, smooth muscle cell(s); PKC, protein kinase C; LDL modification; MC, monocytic cell(s); Signalling; α-TOH, α-tocopherol; Vascular biology; PLA 2, phospholipase A 2; WHHL, Watanabe heritable hyperlipidemic (rabbit); O 2 − , superoxide (anion); EC, endothelial cell(s); IL, interleukin; PPARγ, peroxisome proliferator-activated receptor-γ; α-TOS, α-tocopheryl succinate; MCP1, monocyte chemoattractant protein-1; Vascular disease; Human; Lipoprotein LDL; Pathophysiology; Atherosclerosis; Cardiovascular disease; Exploration; Review; E-Vitamins
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/S0021-9150(00)00741-3

Athersclerosis is a disease involving both oxidative modifications and disbalance of the immune system. Vitamin E, an endogenous redox-active component of circulating lipoproteins and (sub)cellular membranes whose levels can be manupulated by supplementation, has been shown to play a role in the initiation and progression of the disease. Recent data reveal that the activities of vitamin E go beyond its redox function. Moreover, it has been shown that vitamin E can exacerbate certain processes associated with atherogenesis. In this essay we review the role of biology of atherosclerosis, and suggest that these two facets decide the clinical manifestation and outcome of the disease.