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Atherosclerosis pathogenesis includes mechanisms such as hyperglycemia, nonenzymatic glycosylation of lipids, activation of signaling pathways leading to the generation of proinflammatory cytokines/chemokines, and enhanced oxidative stress [63]

In the endothelium of blood vessel walls, long-term high SUA-related ROS attacks significantly increase the expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin on endothelial cells, enhancing lipid permeability

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Thioredoxin-interacting protein mediates ER stress-induced cell death through initiation of the inflammasome