Monocyte chemotactic protein-1 (MCP-1) (also referred to as chemokine (C-C motif) ligand 2 (CCL2) is expressed by mainly inflammatory cells and endothelial cells. The expression level is upregulated after proinflammatory stimuli and tissue injury which are associated with atherosclerotic lesion. Atherosclerosis is a progressive disease starting with accumulation of lipids, lipoproteins, and immune cells in the arterial wall. MCP-1 has been reported to play an important role in the pathogenesis of atherosclerosis and considerable evidence supports that the monocyte containing MCPs and macrophage influences the growth of other cell types within the atherosclerotic lesion. This review will focus on the general structure features of MCP-1 and its role in atherosclerosis.

Atherosclerosis is driven by inflammation with an involvement of innate and adaptive immune responses. Toll-like receptors, the well-defined pattern recognition receptors of the immune system, play a central role in macrophage activation. Toll-like receptors recognize pathogen-associated molecular patterns expressed by a wide range of infectious agents and provide a strong link between local innate and adaptive immunity. Activation of these receptors triggers an intracellular signaling cascade mediated through myeloid differentiation factor 88 or toll/interleukin-1 receptor-domain-containing adapter-inducing interferon-β, leading to the secretion of proand anti-inflammatory cytokines. Engagement of Toll-like receptors with their ligands induces leukocyte recruitment and enhances matrix metalloproteinase expression within atherosclerotic lesions. Recently certain Toll-like receptors have shown a protective role in atherosclerosis. TLRs, therefore, represent an important link between inflammation and atheroma, making them attractive targets for the treatment of atherosclerosis. This review will briefly describe the general biological structure and potential roles of Toll-like receptors as therapeutic targets for the treatment of atherosclerosis and highlight the potential challenges on Toll-like receptor- based therapy in cardiovascular disease.

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