Role of plasma cholesterol in atherosclerosis

An elevation in plasma total cholesterol appears to be one of the major risk factors for atherosclerosis (for review, see Grundy, 1986a). Experimental evidence indicates that decreasing plasma cholesterol can reduce the progression and even induce regression of the atheroslcerotic 

The surface of the lipoproteins in plasma contains the apolipoproteins which determine the ultimate fate of the individual lipoproteins due to their interaction with enzymes and receptors on various cells in the body. The clearance of LDL from plasma is accomplished via the interaction of apo B on LDL with the LDL receptor on various peripheral tissues and liver. Apo B is also considered a risk factor for coronary heart disease (Sniderman, 1988). The presence of apo Ai on the surface of HDL may account for the protective role of this lipoprotein. The apo B/apo Aj ratio may be a better indicator of risk than apo B alone (Thompson, 1984). 

In hypercholesterolemic patients, LDL uptake by tissues is inhibited due to an inherited defect or absence of LDL receptors resulting in extremely high levels of plasma total and LDL-cholesterol (Brown and Goldstein, 1986). Cholesterol from LDL is deposited into blood vessels by a scavenger method and may contribute to the development of atherosclerosis in these individuals. Altered LDL particles can also be taken up by macrophages via a modified receptor method preferentially over the LDL receptor method in tissues. This may lead to the development of foam cells and fatty streaks in the blood vessels, early indicators of the atherosclerotic process (Steinberg et al., 1989). 

---