Modifications and Degradation of High Density Lipoproteins

Abstract

Plasma high density lipoproteins (HDL) attract wide interest because of their putative antiatherogenic role in man (1). It has been repeatedly demonstrated that the plasma concentration of HDL cholesterol correlates inversely with coronary disease risk and this is true for both men and women (2). This protective effect of HDL is independent of total plasma cholesterol levels and is thus viewed as a risk predictor independent of all other lipoprotein classes. Reduced plasma HDL cholesterol levels are associated with a large number of clinical states and the list continues to grow. In Table 1, both genetic and acquired diseases where HDL cholesterol are frequently reduced with increased risk for coronary heart disease is shown. Tempting as it is to attribute causality to the HDL particle per se, the precise mechanism or mechanisms responsible for the protection associated with this lipoprotein has not been determined. It is evident that until all the relevant functional properties of HDL as it circulates in the plasma and extravascular compartments are well understood, the mechanism underlying its antiatherogenic properties shall remain a mystery. Furthermore, because HDL are formed and degraded by complex mechanisms involving turnover of constituent elements, an understanding of these processes is also necessary as background to a discussion of degradation of this species.