Adipose tissue and vascular inflammation in coronary artery disease

Table 1 Possible link of resistin, C-reactive protein and apelin with vascular inflammation, atherosclerosis and cardiovascular diseas

Adipokine	Modulation of inflammation	Association with CVD
Leptin	↑ T cell activation and Th lymphocyte response ↑ cytokine release ↑ NK cell activation ↑ macrophages’ cytokine release Activates neutrophils ↑ chemotaxis ↑ oxidative stress ↑ CRP production from endothelium	↑ blood pressure ↑ atherothrombosis: ↑ cholesterol accumulation in vessel wall ↑ adhesion molecules (ICAM, VCAM) expression ↑ endothelial dysfunction (increasing eNOS production, ↓ NO, ↑ET-1) ↑ proliferation and migration of EC and VSMC ↑ ROS accumulation ↑ VSMC apoptosis ↓ angiogenesis ↑ platelet activity ↓ fibrinolysis ↑ PAI-1 ↑TF release from mononuclear cells Induce insulin resistance
Adiponectin	↓ T cell activation and proliferation ↓ NF-κB Increases IL-10 Inhibits CRP and IL-6 release	Associated with HDL-C and inversely with LDL-C ↓ atherothrombosis: ↓ ICAM-1, VCAM-1, and E-selectin ↓ Transformation of macrophages to foam cells ↓ vascular muscular smooth cells proliferation and migration ↑ TIMP, through the increase in IL-10 ↑ oxidation of free fatty acids in several tissue ↑ insulin sensitivity

CVD: Cardiovascular disease; CRP: C-reactive protein; EC: Endothelial cells; ET-1: Endothelin-1; ICAM: Intercellular adhesion molecule; HDL-C: High density lipoprotein cholesterol; IL: Interleukin; LDL-C: Low density lipoprotein cholesterol; NF-κB: Nuclear factor κB; NK: Natural killer; NO: Nitric oxide; PAI-I: Plasminogen activator inhibitor-I; TF: Tissue factor; TIMP: Tissue inhibitor of metalloproteinase; VCAM: Vascular cell adhesion molecule; VSMC: Vascular smooth muscle cells.