[Cellular and molecular bases of cholesterol accumulation in the vascular wall and its contribution to the progression of atherosclerotic lesion].

The rupture of atherosclerotic plaques depends mainly on their composition. 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/macrophages. Although some of them, especially in advanced plaques, derive from smooth muscle cells. Different receptors involved in the process of foam cell formation have been identified: e.g., scavenger receptors, VLDL receptors and alpha 2-macroglobulin/low density lipoprotein receptor-related proteins. The LDL derived cholesterol collected by these receptors is transformed through the enzyme acyl CoA cholesterol acyl transferase (ACAT) in esterified cholesterol, the hallmark of foam cell formation. High density lipoprotein (HDL) allows the release of free cholesterol from the plasmatic membrane inducing the regression of atherosclerotic lesions.