Fig. 4

S100A12 is closely related to the onset and development of inflammation. The interaction of S100A12 with RAGE activates inflammatory cells such as macrophages and lymphocytes. When macrophages absorb lipids, they form foam cells that participate in the formation of atherosclerotic lesions. In addition, the interaction of S100A12 with TLR4 activates monocytes and induces an inflammatory response. Activated NF-κB and MAPK pathways produce a large number of pro-inflammatory cytokines (TNF-α, IL-1β) and adhesion molecules (VCAM-1, ICAM-1) and downregulate the expression of the anti-apoptotic protein Bcl-2 and upregulate the expression of pro-apoptotic proteins Bax, caspase-3, and caspase-9, leading to cell apoptosis and vascular calcification