CELLULAR AND MOLECULAR-BASIS OF CHOLESTEROL ACCUMULATION IN THE ARTERIAL-WALL - CONTRIBUTION TO THE PROGRESSION OF ATHEROSCLEROTIC LESIONS

The rupture of atherosclerotic plaques depends mainly on their composi tion. Vulnerable plaques are those that contain a large Lipidic core, which derives either from the retention and modification of LDL and/or from necrosis of foam cells. Most foam cells derive from monocyte/mac rophages. Although some of them, especially in advanced plaques, deriv e from smooth mucle cells. Different receptors involved in the process of foam cell formation have been identified: e.g., scavenger receptor s, VLDL receptors and alpha(2)-maeroglobulin/low density Lipoprotein r eceptor-related proteins. The LDL derived cholesterol collected by the se receptors is transformed through the enzyme acyl CoA cholesterol ac yl transferase (ACAT) in esterified cholesterol, the hallmark of foam cell formation. High density lipoprotein (HDL) allows the release of f ree cholesterol from the plasmatic membrane inducing the regression of atherosclerotic lesions.