Uric acid is the end product of
purine metabolism in humans.
Hyperuricemia is a
metabolic disease caused by the increased formation or reduced excretion of serum
uric acid (SUA). Alterations in SUA homeostasis have been linked to a number of diseases, and
hyperuricemia is the major etiologic factor of
gout and has been correlated with
metabolic syndrome,
cardiovascular disease, diabetes,
hypertension, and renal disease. Oxidative stress is usually defined as an imbalance between
free radicals and
antioxidants in our body and is considered to be one of the main causes of cell damage and the development of disease. Studies have demonstrated that
hyperuricemia is closely related to the generation of
reactive oxygen species (ROS). In the human body,
xanthine oxidoreductase (XOR) catalyzes the oxidative hydroxylation of
hypoxanthine to
xanthine to
uric acid, with the accompanying production of ROS. Therefore, XOR is considered a
drug target for the treatment of
hyperuricemia and
gout. In this review, we discuss the mechanisms of
uric acid transport and the development of
hyperuricemia, emphasizing the role of oxidative stress in the occurrence and development of
hyperuricemia. We also summarize recent advances and new discoveries in XOR inhibitors.