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Atherosclerosis: cell biology and lipoproteins: C-reactive protein is a biomarker of atherosclerosis and mediator of plaque formation.

Atherosclerosis is a complex disease process initiated by infiltration of low-density lipoproteins (LDLs) into the subendothelial space where they accumulate and become modified mainly by oxidation [1 ]. The oxidative stress on the endothelium leads to a cascade of inflammatory reactions which potentiates the development of atheromatous plaque and further disease progression. High-sensitivity C-reactive protein (CRP), a marker of systemic inflammation, has been identified as a predictive marker of cardiovascular events. CRP exerts numerous effects on endothelial biology that favours a proatherosclerotic phenotype such as decreasing nitric oxide release, upregulating adhesion molecules, stimulating vascular smooth muscle cell proliferation and migration, and activating the complement system [2]. CRP also enhances the expression of interleukin 6, monocyte chemoattractant protein 1 (MCP-1), plasminogen activator inhibitor 1 (PAI-1), endothelin 1 and cell-adhesion molecules in the endothelial cells [3]. CRP binds to a large number of autologous and extrinsic ligands, including native and modified plasma lipoproteins, phospholipids and apoptotic cells, present in atherosclerotic lesions [4]. Chemokines, particularly MCP-1, play a key role in migration of monocytes and T-cells into the walls of blood vessels and in the evolution of atherosclerosis. Increasing levels of PAI-1 in the vessel wall promotes the formation of rupture-prone plaques with lipid-laden cores and thin fibrous caps [5,6].