[Cholesterol metabolism in the arteriosclerotic intima]

Cholesterol and cholesteryl esters play an active role in the metabolism of intimal cells which are involved in the arteriosclerotic process (macrophages derived from monocytes and smooth muscle cells). LDL is the main carrier protein of both lipids and enters the vessel wall to become retained. Macrophages in cell culture have been shown to internalise LDL in an irregular fashion, if LDL is modified by oxidation, by formation of complexes with proteoglycans, malondialdehyde, etc. The development of foam cells in the intima may be interpreted in this way. Lipid-laden smooth muscle cells appear as well. Importance must be attributed to the processes of lysosomal hydrolysis of cholesteryl esters and subsequent re-esterification and hydrolysis of these lipids in cytoplasma. The free cholesterol delivered in this way may be transported by a carrier protein to the cell surface, taken up by the cholesterol acceptor HDL, and removed from the vessel wall. Phospholipids and apo E take part in this cholesterol reverse transport. But the ability of arterial tissue to release cholesterol is limited. Extracellular precipitations of cholesterol occur in the lipid accumulations which are sclerogenic. In advanced ulcerated arteriosclerosis they are the source of cholesterol crystal embolization. Cholesteryl esters extruded in the extracellular space by lysis of foam cells are taken up by monocyte-derived macrophages after interaction with albumin or fibronectin which function as opsonins.