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. 2013 Dec 22;2013:828354. doi: 10.1155/2013/828354

Figure 1.

Figure 1

Overview of the interplay between S100A8/A9, traditional CV risk factors, circulating phagocytes, and atherogenesis. Smoking, hyperlipidemia, hyperglycemia, and obesity induce elevated S100A8/A9 production either directly or indirectly by stimulating neutrophilia and monocytosis. S100A8/A9 enhances phagocyte production in the bone marrow and facilitates their recruitment into the vascular wall through endothelial activation and increased Mac-1 expression and affinity. These effects are primarily mediated by RAGE and accelerated by hyperglycemia. In the vascular wall, S100A8/A9 binding to TLR4 triggers phagocyte activation and secretion of inflammatory cytokines, further contributing to phagocyte recruitment and accelerated atherogenesis. M-CSF: macrophage colony stimulating factor; GM-CSF: granulocyte-macrophage colony stimulating factor; RAGE: receptor for advanced glycation end products; TLR4: toll-like receptor 4.