Uric Acid Induces Endothelial Dysfunction by Activating the HMGB1/RAGE Signaling Pathway

Figure 5

Potential mechanism of UA-induced inflammation in endothelial cell. High uric acid stimulates the RAGE signaling pathway and activates NF-κB, which results in the production and release of proinflammatory cytokines, including the expression and extracellular release of HMGB1 in endothelial cells. As a high affinity ligand of RAGE, HMGB1 interacts with RAGE and contributes to the amplification of the inflammatory response and finally induces endothelial dysfunction. Blockade of RAGE by anti-RAGE antibody can suppress the HMGB1/RAGE signaling pathway, therefore alleviating endothelial dysfunction.