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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.