Table 1

Proposed mechanisms by which high-density lipoproteins (HDLs) influence atherosclerosis

Normal protective HDLs

Proinflammatory HDLs


Reverse cholesterol transport

Impaired reverse cholesterol transport

ApoAI and other lipoproteins in HDLs transport cholesterol from artery walls and macrophages to other lipids and to the liver for recycling or disposal

ApoAI and apoJ are disabled after the addition of chlorine, nitrogen, and/or oxygen

Lipoprotein synthesis is reduced by inflammation

Antioxidant activities

Pro-oxidant activities

Due primarily to enzymes PON1, lecithin cholesterol acyltransferase, platelet-activating acyl hydrolase, and glutathione peroxidase

PON1 is disabled by association with altered apoAI

Synthesis of enzymes is decreased by inflammation

Pro-oxidants serum amyloid A and ceruloplasmin are added to HDLs

Anti-inflammatory activities

Proinflammatory activities

Prevent generation of oxidized LDLs and oxidation of other proinflammatory lipids

Primarily promote oxidation of LDLs

Prevent endothelial cells from expressing monocyte chemotactic protein-1 and other chemoattractants

Diminish interactions between T cells and monocytes


apo, apolipoprotein; LDL, low-density lipoprotein; PON, paraoxonase.

Hahn et al. Arthritis Research & Therapy 2008 10:213   doi:10.1186/ar2471