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Hyperlipidemia Foam cells

NO also reduces endothelial adhesion of monocytes and leukocytes, key features of the early development of atheromatous plaques. This effect is due to the inhibitory effect of NO on the expression of adhesion molecules on the endothelial surface. In addition, NO may act as an antioxidant, blocking the oxidation of low-density lipoproteins and thus preventing or reducing the formation of foam cells in the vascular wall. Plaque formation is also affected by NO-dependent reduction in endothelial cell permeability to lipoproteins. The importance of eNOS in cardiovascular disease is supported by experiments showing increased atherosclerosis in animals deficient in eNOS by pharmacologic inhibition. Atherosclerosis risk factors, such as smoking, hyperlipidemia, diabetes, and hypertension, are associated with decreased endothelial NO production, and thus enhance atherogenesis. [Pg.422]

Plaque ruptures in the ACS setting are often involved with a diffuse process, Inflammation is involved in plaque growth and development in addition to complications of plaque rupture. These could be considered the result of injury, Well-known coronary risk factors can provide the impetus for plaque development. Cigarette smoking, hypertension, hyperlipidemia, hyperglycemia, or insulin resistance are noxious stimuli. The stimuli can facilitate monocyte attachment to endothelial cells. Eventually monocytes migrate to the subintimal space and become foam cells to initiate plaque development. [Pg.469]

Ascorbate supplementation prevents the exacerbation of CVD associated with hypertriglyceridemia. Type III hyperlipidemia, and related disorders by stimulating lipoprotein lipases and thereby enabling a normal catabolism of triglyceride-rich lipoproteins." Ascorbate prevents the oxidative modification of these lipoproteins, their uptake by scavenger cells and foam cell formation. Moreover, we propose here that, analogous to the LDL receptor, ascorbate also increases the expression of the receptors involved in the metabolic clearance of triglyceride-rich lipoproteins, such as the chylomicron remnant receptor. [Pg.621]

The compound 6,7-dimethoxycoumarin or scoparone isolated from the herb Artemisia scoparia possesses vasodilator and hypolipidemic effects and has been tested in rabbits with hyperhpidemia and diabetogenic condition. Administration of this coumarin for a week was able to reduce total cholesterol and triglycerides to normal values. Furthermore, scoparone treatment retarded the characteristic pathomorphological changes associated with hyperlipidemia such as intimal thickening or accumulation of fatty streaks and foam cells [264]. [Pg.189]


See other pages where Hyperlipidemia Foam cells is mentioned: [Pg.209]    [Pg.209]    [Pg.127]    [Pg.127]    [Pg.260]   


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