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However, cellular malfunction and mortality are caused by oxidative stress and mitochondrial dysfunction [4]

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Elevated SUA activates endothelial NF-B signaling, upregulating monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) expressions to accelerate atherosclerosis progression ( This metabolic disturbance demonstrates bidirectional interactions with components of metabolic syndrome

These drugs include torcetrapib, dalcetrapib, evacetrapib, and niacin [68], (Fig

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Mol Biochem Parasitol 1996