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Archives of cardiovascular diseases
Volume 106, n° 11
pages 601-611 (novembre 2013)
Doi : 10.1016/j.acvd.2013.06.052
Received : 15 Mars 2013 ;  accepted : 27 June 2013
Targeting high-density lipoproteins: Update on a promising therapy
Les HDL comme cible thérapeutique : état des lieux
 

Figure 1




Figure 1 : 

Pleiotropic protective effects of high-density lipoprotein (HDL). Green text indicates pleiotropic effects. Red text indicates HDL components or mechanisms responsible for these biological effects. Apo: apolipoprotein; ATP: adenosine triphosphate; BAD: Bcl-2-associated death promoter; BAX: Bcl-2-associated X protein; ICAM: intercellular adhesion molecule; LDL: low-density lipoprotein; NO: nitric oxide; PAF-AH: platelet-activating factor-acetyl hydrolase; S1P: sphingosine-1-phosphate; SAA: serum amyloid A protein; SR-BI: scavenger receptor class B type I; VCAM: vascular cellular adhesion molecule.


Figure 2




Figure 2 : 

Possible explanations for the effects of nicotinic acid on lipoprotein profile and protective mechanisms. apo: apolipoprotein; ATP: adenosine triphosphate; CE: cholesterol ester; CETP: cholesteryl ester transfer protein; DGAT: diacylglycerol acyltransferase; HCAR: hydroxycarboxylic acid receptor; HDL: high-density lipoprotein; LDL: low-density lipoprotein; MCP: monocyte chemoattractant protein; P2Y13 : purinergic receptor 13; TG: triglycerides; VCAM: vascular cellular adhesion molecule; VLDL: very-low-density lipoprotein.

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