Dear Colleagues,

Human xanthine oxidoreductase (XOR) is produced by cells as a dehydrogenase (XDH), but it can be converted in vivo into an oxidase (XO). Both activities catalyze the last two steps in the purine catabolism process, generating uric acid and either NADH or reactive oxygen species (ROS). XOR can also act as an NADH oxidase that produces ROS and as a nitrite reductase that generates nitric oxide (NO).

Uric acid is a fundamental antioxidant molecule in serum. In addition, it is recognized by macrophages as a damage-associated molecular pattern, has a neurostimulator effect, supports blood pressure, and promotes fat accumulation. XOR-produced ROS and NO play a physiological role in signal transduction by contributing to vasodilation and the regulation of blood pressure. In addition, these XOR products trigger a microvascular inflammatory response and are essential for the cytocidal activity of leukocytes as well as the control of intestinal bacterial flora.

However, an increased amount of serum XOR has been reported in various liver pathologies and, in turn, can be responsible for oxidative stress. Hyperuricemia often leads to gout and is involved in hypertension, which promotes cardiovascular, kidney, and metabolic diseases, which are also fostered by oxidative stress. The implications of XOR activities and products have been suggested in chronic inflammation and the aging process, as well as in tumor transformation and progression.

Various drugs are available to inhibit XOR activity or simply lower uricemia, but the effects of these drugs are still uncertain. Currently, more specific multivariate meta-analyses are needed to evaluate when and which urate-lowering therapy can be recommended.

We would like to invite you to submit your latest research findings, clinical studies, or review articles to this Special Issue focusing on the biology of XOR and the involvement of its products in human pathology, as well as the pharmacological control of its activity.

Prof. Dr. Maria Giulia Battelli
Prof. Dr. Andrea Bolognesi
Guest Editors

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• cancer
• endothelium dysfunction
• hyperuricemia
• inflammation
• nitric oxide
• oxidative stress
• reactive oxygen species
• uric acid
• xanthine dehydrogenase
• xanthine oxidase
• xanthine oxidoreductase