Abstract
The oxidation of low density lipoprotein (LDL) is one of the key-events in the initiation and progression of the atherosclerotic disease1, 2. Oxidized LDL exerts a series of biological effects that make it more atherogenic than its parent form. Among them is cytotoxicity to endothelial and smooth muscle cells3,4. The mechanisms underlying the cytotoxic effect of oxidized LDL are still under active investigation, and the biochemical identification of the factor(s) responsible for oxLDL-mediated cytotoxicity is far to be exhaustively performed. In fact, the oxidation of LDL particles generates a mixture of compounds with potential cytotoxic activity, including a variety of cholesterol oxides5. Among them, cholestane-3β,5α,6β-triol (CH), 5-cholesten 3β-ol-7one (KC), and 25-OH-cholesterol (COH) have received particular attention since they are generated in vivo6,7,8. Cholesterol oxide-mediated cytotoxicity has been investigated in both endothelial and smooth muscle cells9,10,11, and CH has been reported to affect the barrier fonction of the endothelial layer9.
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Palladini, G., Bellomo, G. (1996). Alterations of Vimentin-Nucleus Interactions as an Early Phase in Cholesterol Oxide - Induced Endothelial Cell Damage. In: Slavík, J. (eds) Fluorescence Microscopy and Fluorescent Probes. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1866-6_37
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DOI: https://doi.org/10.1007/978-1-4899-1866-6_37
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