Abstract
A growing bulk of evidence suggests that cholesterol oxidation products, known as oxysterols, and 4-hydroxy-2-nonenal (HNE), the major proatherogenic components of oxidized low density lipoproteins (oxLDLs), significantly contribute to atherosclerotic plaque progression and destabilization, with eventual plaque rupture. These oxidized lipids are involved in various key steps of this complex process, mainly thanks to their ability to induce inflammation, oxidative stress, and apoptosis. This review summarizes the current knowledge of the effects induced by these compounds on vascular cells, after their accumulation in the arterial wall and in the atherosclerotic plaque.
Keywords:
Atherosclerosis; HNE; Oxysterols.
Copyright © 2017 Elsevier Inc. All rights reserved.
MeSH terms
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Aldehydes / metabolism*
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Animals
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Apoptosis
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Arachidonate 5-Lipoxygenase / genetics
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Arachidonate 5-Lipoxygenase / metabolism
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Cytokines / genetics
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Cytokines / metabolism
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Disease Progression
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Endothelial Cells / metabolism*
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Endothelial Cells / pathology
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Gene Expression Regulation
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Humans
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Lipoproteins, LDL / metabolism*
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NF-kappa B / genetics
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NF-kappa B / metabolism
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Oxidative Stress
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Oxysterols / metabolism*
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Plaque, Atherosclerotic / genetics
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Plaque, Atherosclerotic / metabolism*
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Plaque, Atherosclerotic / pathology
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Signal Transduction
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p38 Mitogen-Activated Protein Kinases / genetics
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p38 Mitogen-Activated Protein Kinases / metabolism
Substances
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Aldehydes
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Cytokines
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Lipoproteins, LDL
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NF-kappa B
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Oxysterols
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oxidized low density lipoprotein
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Arachidonate 5-Lipoxygenase
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p38 Mitogen-Activated Protein Kinases
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4-hydroxy-2-nonenal