“…Macrophages and foam cells present in the evolving atherosclerotic lesion, secrete various proinflammatory cytokines, such as TNF-α, IFN-γ, IL-6, and chemokines, including ICAM-1 and VCAM-1. In response to enhanced production of proinflammatory cytokines, endothelial cells express high levels of leukocyte adhesion molecules on their surface, leading to further mononuclear cell recruitment and, hence, to development of a chronic inflammatory state [21][22][23] .…”