Figure 4. Alterations of the atheroprotective effects of HDL in patients with CAD.

Modification of apoA-I by MPO has been shown to impair the macrophage cholesterol efflux capacity of HDL. More recently, accumulation of MDA in HDL from patients with CAD due to an impaired HDL-associated PON1 activity has been observed to stimulate activation of endothelial PKCbeta-II via the LOX-1 receptor. PKCbeta-II activation by HDL from patients with CAD inhibited Akt-dependent phosphorylation of eNOS at serine residue 1177 and increased the inhibitory eNOS phosphorylation at threonine 495, leading to reduced endothelial NO production.