The objective of this study was to investigate the influence of the APOE promoter (-491 A/T, -427 T/C and -219 G/T) and coding region (APOE epsilon2/epsilon3/epsilon4) polymorphisms in atherosclerosis disease by association and linkage disequilibrium analyses.
We conclude that the APOE*4 allele is associated with an increased risk for atherosclerotic vascular disease, that this association has an age-dependent effect, and that it acts as a genetic factor that increases susceptibility to developing the disease in young to middle-aged male adults in our population.
This ability of APOE4/4 VLDL to inhibit the antiapoptotic effects of HDL presents a potential mechanism by which the expression of several diseases, including atherosclerosis, is enhanced by the APOE4 genotype.
In the present study, we evaluated whether accelerated atherosclerosis in human vein grafts could be mimicked in hypercholesterolemic APOE*3 Leiden transgenic mice.
In apoE4-negative subjects, the progression of atherosclerosis severity score was significantly faster in control than in the HRT groups (genotype-by-time interaction P = 0.0026); whereas in apoE4-positive subjects, there were no significant differences in atherosclerosis severity score progression between the control and HRT groups.