Tags

Type your tag names separated by a space and hit enter

Relationships among hyperuricemia, endothelial dysfunction and cardiovascular disease: molecular mechanisms and clinical implications.
J Cardiol. 2012 May; 59(3):235-42.JC

Abstract

Uric acid is the end product of purine metabolism. Its immediate precursor, xanthine, is converted to uric acid by an enzymatic reaction involving xanthine oxidoreductase. Uric acid has been formerly considered a major antioxidant in human plasma with possible beneficial anti-atherosclerotic effects. In contrast, studies in the past two decades have reported associations between elevated serum uric acid levels and cardiovascular events, suggesting a potential role for uric acid as a risk factor for atherosclerosis and related diseases. In this paper, the molecular pattern of uric acid formation, its possible deleterious effects, as well as the involvement of xanthine oxidoreductase in reactive oxygen species generation are critically discussed. Reactive oxygen species contribute to vascular oxidative stress and endothelial dysfunction, which are associated with the risk of atherosclerosis. Recent studies have renewed attention to the xanthine oxidoreductase system, since xanthine oxidoreductase inhibitors, such as allopurinol and oxypurinol, would be capable of preventing atherosclerosis progression by reducing endothelial dysfunction. Also, beneficial effects could be obtained in patients with congestive heart failure. The simultaneous reduction in uric acid levels might contribute to these effects, or be a mere epiphenomenon of the drug action. The molecular mechanisms involved are discussed.

Authors+Show Affiliations

Department of Internal Medicine, Aging and Nephrological Diseases, University of Bologna and S. Orsola-Malpighi Hospital, Bologna, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

22398104

Citation

Puddu, Paolo, et al. "Relationships Among Hyperuricemia, Endothelial Dysfunction and Cardiovascular Disease: Molecular Mechanisms and Clinical Implications." Journal of Cardiology, vol. 59, no. 3, 2012, pp. 235-42.
Puddu P, Puddu GM, Cravero E, et al. Relationships among hyperuricemia, endothelial dysfunction and cardiovascular disease: molecular mechanisms and clinical implications. J Cardiol. 2012;59(3):235-42.
Puddu, P., Puddu, G. M., Cravero, E., Vizioli, L., & Muscari, A. (2012). Relationships among hyperuricemia, endothelial dysfunction and cardiovascular disease: molecular mechanisms and clinical implications. Journal of Cardiology, 59(3), 235-42. https://doi.org/10.1016/j.jjcc.2012.01.013
Puddu P, et al. Relationships Among Hyperuricemia, Endothelial Dysfunction and Cardiovascular Disease: Molecular Mechanisms and Clinical Implications. J Cardiol. 2012;59(3):235-42. PubMed PMID: 22398104.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Relationships among hyperuricemia, endothelial dysfunction and cardiovascular disease: molecular mechanisms and clinical implications. AU - Puddu,Paolo, AU - Puddu,Giovanni M, AU - Cravero,Eleonora, AU - Vizioli,Luca, AU - Muscari,Antonio, Y1 - 2012/03/06/ PY - 2011/12/19/received PY - 2012/01/17/revised PY - 2012/01/20/accepted PY - 2012/3/9/entrez PY - 2012/3/9/pubmed PY - 2013/3/8/medline SP - 235 EP - 42 JF - Journal of cardiology JO - J Cardiol VL - 59 IS - 3 N2 - Uric acid is the end product of purine metabolism. Its immediate precursor, xanthine, is converted to uric acid by an enzymatic reaction involving xanthine oxidoreductase. Uric acid has been formerly considered a major antioxidant in human plasma with possible beneficial anti-atherosclerotic effects. In contrast, studies in the past two decades have reported associations between elevated serum uric acid levels and cardiovascular events, suggesting a potential role for uric acid as a risk factor for atherosclerosis and related diseases. In this paper, the molecular pattern of uric acid formation, its possible deleterious effects, as well as the involvement of xanthine oxidoreductase in reactive oxygen species generation are critically discussed. Reactive oxygen species contribute to vascular oxidative stress and endothelial dysfunction, which are associated with the risk of atherosclerosis. Recent studies have renewed attention to the xanthine oxidoreductase system, since xanthine oxidoreductase inhibitors, such as allopurinol and oxypurinol, would be capable of preventing atherosclerosis progression by reducing endothelial dysfunction. Also, beneficial effects could be obtained in patients with congestive heart failure. The simultaneous reduction in uric acid levels might contribute to these effects, or be a mere epiphenomenon of the drug action. The molecular mechanisms involved are discussed. SN - 1876-4738 UR - https://www.unboundmedicine.com/medline/citation/22398104/Relationships_among_hyperuricemia_endothelial_dysfunction_and_cardiovascular_disease:_molecular_mechanisms_and_clinical_implications_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0914-5087(12)00019-6 DB - PRIME DP - Unbound Medicine ER -