This results in a progressive amplification of endothelial dysfunction and the further release of inflammatory cytokines (notably IL-6, Interleukin-6), chemokines (notably, MCP-1, monocyte chemoattractant protein-1), growth factors (notably, TGFβ, transforming growth factor beta) and vasoconstricting mediators such as 5-HT (5-hydroxytryptamine) [16,35,36]. This evidence concerns the gene CCL2 and endothelial dysfunction.