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Lipid Physiology
iride6606 posted:
Here is a great summary of the physiology of lipids (ie cholesterol) and how they contrubute to the development atherosclerotic lesions. Excerpt;

Chylomicron remnants are removed in the liver by species that bind apo E: LRP, the LDL receptor, and cell surface glycosaminoglycans. Chylomicrons are large, and it is unlikely that they contribute to atherosclerosis. Chylomicron remnants are enriched in cholesteryl esters, the major lipid component of the atherosclerotic lesion, and small enough to enter the subendothelial space, where they are taken up by macrophages. Remnants are atherogenic, consistent with the idea that the progression of atherosclerotic lesions can occur in the postprandial state, a potential contributor to morbidity not assessed by current practices that focus on the measurement of fasting lipoproteins.

LDL enters the subendothelial space of the vascular wall, where its modification by oxidation or other processes promotes its uptake by macrophages in atherosclerotic lesions.

Really intersting stuff, explains how the physiology of cholesterol contributes to atherosclerotic lesions. As you can see, as long as the physiology of cholesterol goes unchanged, it will continue to be a risk factor in developing CAD.

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