Cellular, molecular and clinical aspects of vitamin E on atherosclerosis prevention

Munteanu, Adelina; Zingg, Jean‐Marc

doi:10.1016/j.mam.2007.07.001

Cited by 68 publications

(53 citation statements)

References 410 publications

(392 reference statements)

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“…5 (ie, vitamins E and C) that, when deficient, may further contribute to injury under conditions of inflammatorydriven oxidative stress in the vascular wall. 72,73 Vitamin C or (ascorbic acid) has been shown to provide widespread protection against atherogenesis such as the prevention of endothelial dysfunction, inhibition of dedifferentiation, and proliferation of SMCs, and a reduction in oxLDL uptake and degradation by macrophages. 74 Similarly, vitamin E (tocopherols and tocotrienol derivatives) has been shown to reduce inflammatory markers such as CRP and suppress the release of proinflammatory cytokines plasminogen activator inhibitor (PAI-1) and IL-8.…”

Section: Carbohydratesmentioning

confidence: 99%

Inflammation at the Molecular Interface of Atherogenesis

Lamon

Hajjar

2008

The American Journal of Pathology

112

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Despite the multifactorial nature of atherosclerosis, substantial evidence has established inflammation as an often surreptitious, yet critical and unifying driving force which promotes disease progression. To this end, research has defined molecular networks initiated by cytokines, growth factors and other proinflammatory molecules which promote hallmarks of atherosclerosis such as endothelial dysfunction, macrophage infiltration, LDL oxidation, cell proliferation and thrombosis. Although commonly associated with risk factors such as dyslipidemia, diabetes and hypertension, the global etiology of atherosclerosis may be alternatively attributed to underlying anthropological pressures. The agricultural, industrial and technological revolutions produced alterations in dietary, social and economic factors which have collectively exaggerated the exposure of the human genome to environmental stimuli. Furthermore, advances in sanitation, nutrition, and medicine have increased the lifespan of humans, effectively prolonging blood vessel exposure to these factors. As a result, the vasculature has become conditioned to respond to injury with what is arguably an overzealous immunological response; thus setting the stage for the prevalence of cardiovascular disease, including atherosclerotic plaque development in Western populations. Evidence suggests that each of these alterations can be linked to specific mediators in the inflammatory process. Integration of these factors with an inflammationbased hypothesis of atherosclerosis has yet to be extrapolated to observations in the realms of basic and clinical sciences and is the focus of this review. (Am J Pathol

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Section: Carbohydratesmentioning

confidence: 99%

Inflammation at the Molecular Interface of Atherogenesis

Lamon

Hajjar

2008

The American Journal of Pathology

112

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“…The vit. E can prevent the production of pro-inflammatory cytokines including IL-1, IL-6, TNF and chemokines IL-8 that produced by monocytes and macrophages (Devaraj and Jialal, 1999;Munteanu and Zingg, 2007) and IFN-γ that produced by T cells (Winkler et al, 2007). Magnesium plays an important role in inflammatory disease because lack of magnesium in the body can cause several inflammatory disorders such as type 2 DM (Schulze et al, 2007;Villegas et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Decreasing the Expression Level of Macrophage Cell, Pro-Inflammatory Cytokines and NF-κB by Using VipAlbumin® in vitro

Dwij¹,

Dj²,

Rifa’i³

2015

Asian J. of Cell Biology

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“…A series of studies has drawn attention to the regulatory aspects of α-tocopherol on VSMCs and atherosclerosis (Munteanu & Zingg, 2007). However, the mechanism of action of α-tocopherol has proven difficult to define, owing to its highly lipophilic nature.…”

Section: Discussionmentioning

confidence: 99%