Fig. 8

a Oxidative modification of lipoprotein in the presence of high glucose in the vascular system activates monocytes as well as the endothelial cells facilitating adhesion of circulating monocytes. Activated endothelial cells secrete chemokines and promote monocyte rolling, tethering and then transmigration into the subendothelial space. b These monocyte then firmly adhere to the endothelial cells and differentiate into macrophages. Macrophages engulf oxidised lipoproteins to form foam cells. These modifications incite an inflammatory response and result in an increase in the levels of cytokines such as MCP-1, TNF-α and extracellular cyclophilin A. c When monocyte derived macrophages are treated with either siRNA or chemical inhibitor TMN 355, to silence/inhibit cyclophilin A it leads to a decrease in expression of CD36 and LOX-1 indicating reduced monocyte-macrophage differentiation as well as reduced lipid uptake. The levels of inflammatory cytokines, MCP-1, TNF-α and cyclophilin A also decreases. This highlights the role of cyclophilin A in promoting vascular inflammation in hyperglycemia