Dysfunctional HDL Causes Platelet Apoptosis and Accelerated Thrombogenesis

Our previous study suggests that the HDL from patients with Familial Hypercholesterolemia (FH) is enriched with peroxidation products, including malondialdehyde (MDA) and isolevuglandins (IsoLG), and is strikingly dysfunctional and enhances platelet abnormalities leading to atherosclerosis, yet the mechanisms are not clear. Although HDL are regarded as one of the most potent anti-apoptotic factors and oxidized HDL act as pro-apoptotic in macrophages and endothelial cells, little is known about their effect on platelets survival and susceptibility to apoptosis.

Therefore, in our present study, we hypothesize that the maintenance of platelet integrity and protection against potentially deleterious proatherogenic stimuli may constitute a new biological function of HDL and thus may define a new mechanism contributing to their atheroprotective function in FH subjects.