CCL2 and metabolic syndrome: As increased circulating levels of TNFα have been detected in metabolic syndrome patients [12,15], which can up-regulate CX3CL1 expression and promote the generation and release of CCL2 [30,31], we also investigated the role of CX3CL1/CX3CR1 and CCL2/CCR2 axes in platelet-leukocyte and leukocyte adhesion to the dysfunctional arterial endothelium in a metabolic syndrome model.