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Table 1 Proposed mechanisms by which high-density lipoproteins (HDLs) influence atherosclerosis

From: Altered lipoprotein metabolism in chronic inflammatory states: proinflammatory high-density lipoprotein and accelerated atherosclerosis in systemic lupus erythematosus and rheumatoid arthritis

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