Targeting the anti-inflammatory effects of high-density lipoprotein.
The effects of systemic inflammation can impair the anti-inflammatory functions of high-density lipoprotein (HDL) particles. In patients with atherosclerosis and/or inflammatory conditions, HDLs can be modified such that they paradoxically increase the recruitment and activation of macrophages, upregulate the expression of endothelial cell adhesion molecules, and participate in the oxidation of low-density lipoproteins (LDLs). Statins, apolipoprotein A-I mimetic peptides, and therapeutic lifestyle changes appear to mitigate these proinflammatory features of HDLs. In the future, characterizing and targeting functional aspects of HDLs may prove to offer therapeutic advantages over current treatment strategies.
Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, USA. BAnsell@mednet.ucla.edu
Benjamin J
BJ
Ansell
D050197:Atherosclerosis / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D018836:Inflammation Mediators / Q000502:physiology*; D008075:Lipoproteins, HDL / Q000502:physiology*; D010084:Oxidation-Reduction
D018836:Inflammation Mediators; D008075:Lipoproteins, HDL