This newer, more careful understanding of the complex changes that can alter the functionality of both the lipidome and the proteome of HDL particles so that they become dysfunctional, or subfunctional, leads to a second major new concept in HDL biology: that the dynamic intravascular metabolism of both the lipid and the protein components of HDL may be perturbed in cardiometabolic diseases associated with dyslipidemia, inflammation, insulin resistance, and premature CVD, and that taken together, those perturbations result in altered atheroprotective functions of the HDL particles.[11] This leads to the concept that the alterations in the atheroprotective functions of HDL particles are a major factor to be taken into account as we develop new therapeutic agents, not only to correct the concentration of circulating HDL in individuals at high CVD risk, but equally, to normalize the function of those particles in such a way as to afford greater atheroprotection to individuals at risk.
J Clin Lipidol. 2011; 5(6).[11]Chapman MJ, Ginsberg HN, Amarenco P et al; European Atherosclerosis Society Consensus Panel. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur Heart J 2011; 32: 1345-61
