Xanthine oxidoreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications

By C. Berry, J. Hare. Journal of Physiology, 2004

946 citations recorded by the source corpus.

Subfields: Molecular Biology, Nephrology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/dbf724f824002e1fa3cc17092b2908531dfa0690

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In Molecular Biology

1. M. Valko
2. M. Duchen
3. A. Abramov
4. A. Scorziello
5. Richard J. Johnson
6. D. Granger
7. M. Mazúr
8. P. Kvietys

In Nephrology

1. Richard J. Johnson
2. A. Abramov

In Pathology and Forensic Medicine

1. Guy C. Brown
2. Chris E. Cooper

Citations in the corpus

• Chemical and molecular mechanisms of antioxidants: experimental approaches and model systems (2009, background): “Xanthine oxidase (XO) is an enzyme involved in the formation of uric acid in the body, which catalyses the oxidation of hypoxanthine and xanthine to uric acid yielding O2 and H2O2 and raises the oxidative level in an organism (Figure 10) [71].”
• Regulation of uric acid metabolism and excretion. (2016, neutral): “The first regulation of XOR occurs at transcriptional level and its gene expression may be regulated by nutritional factors, steroid hormones, growth factors, cytokines, and insulin [39].”
• Three Distinct Mechanisms Generate Oxygen Free Radicals in Neurons and Contribute to Cell Death during Anoxia and Reoxygenation (2007, background): “Xanthine oxidase inhibitors attenuate brain injury (Palmer et al., 1990) and improve outcome on reperfusion of the heart after bypass surgery (Berry and Hare, 2004).”
• Hyperuricemia induces endothelial dysfunction. (2005, background): “Endothelial dysfunction, particularly impaired nitric oxide production, is a common finding in patients with cardiovascular and renal diseases and is thought to be mediated in part by reactive oxygen species (ROS) [1].”
• Therapeutic Effects of Xanthine Oxidase Inhibitors: Renaissance Half a Century after the Discovery of Allopurinol (2006, background): “…to other cellular and extracellular sources of superoxide) is unclear and, again, may be dependent on many factors, including the species, the cell type, the tissue, and the type and stage of the particular disease (reviewed in Berry and Hare, 2004; Griendling, 2004; Brandes and Kreuzer, 2005).”
• The role of oxidants and free radicals in reperfusion injury. (2006, neutral): “Despite the presence of numerous supporting studies, there have also been negative reports, so that the role of XO in human cardiovascular disease remains controversial and merits further investigation [82].”
• Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, background): “Much attention has been recently devoted to the ability of XO to function as a nitrate/nitrite reductase, which enables the enzyme to catalyze the one electron reduction of nitrite to nitric oxide (NO) [123,145,164].”
• Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities (2011, neutral): “Hydrogen peroxide can also be generated by the 2-electron reduction of oxygen by various oxidoreductases, including xanthine oxidase, which, recent findings suggest, predominately produces hydrogen peroxide (33, 195).”
• Free radicals and antioxidants in normal physiological functions and human disease. (2007, background): “The major sources of oxidative stress in cardiovascular system involve: (i) the enzymes xanthine oxidoreductase (XOR), (ii) NAD(P)H oxidase (multisubunit membrane complexes) and (iii) NOS as well as (iv) the mitochondrial cytochromes and (v) hemoglobin (Berry & Hare, 2004; Hare & Stamler, 2005).”