CCL2 and endothelial dysfunction: Recently, epicardial AT has been shown to have a significant secretory capacity of proinflammatory cytokines, such as interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1), in response to treatment with vasodilator-stimulated phosphoprotein, which is involved in resistin-related endothelial dysfunction [31].