[Contemporary concepts of the role of inflammation in atherosclerosis].

We present in this article main theories of development of atherosclerosis and modern views of the role of inflammation in atherogenesis. We have conducted a review of studies of the role of endothelial local factors such as accumulation of smooth muscle cells, T and B lymphocytes, macrophages, matrix metalloproteinase (MMP), high sensitivity C reactive protein (CRP). It has been shown that low oxidative stress modulates expression of endothelial gene which induces atherogenic factor formatting early atherosclerotic plaque (FP). CRP and oxidized low density lipoproteins (OxLDL) are directly linked with oxidative damage of arteries in ischemic heart disease. Monocytes activated in areas of inflammation by monocyte chemoattractant protein (MCP) 1 and MMP 1 play pivotal role in AP rupture. CRP and OxLDL augment synthesis of MMP, tumor necrosis factor alpha (TNF alpha) and granulocyte macrophage colony stimulating factor (GM CSF). Moreover addition of exogenous MCP 1 and prostaglandin E2 elevates synthesis of MMP 1, TNF alpha, and GM CSF by monocytes. Apoptosis of smooth muscle cells of AP fibrous cap combined with destruction of extracellular matrix proteins by MMP 1 eventually leads to AP rupture.