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Updated: May 1, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
New Insight into Urate-Related Mechanism of Cardiovascular Damage
Davide Grassi1, Giovambattista Desideri, Claudio Ferri
1University of L'Aquila, Department of Life, Health, and Environmental Sciences, Viale S Salvatore, Delta, 6 Medicina, 67100 Coppito, L'Aquila, Italy. davide.grassi@cc.univaq.it.
Abstract:
Several experimental and clinical studies reported that hyperuricemia may trigger hypertension, metabolic syndrome, vascular damage and renal disease. Furthermore, a substantial proportion of epidemiological studies are compatible with the hypothesis that hyperuricemia may be an indipendent risk factor for cardiovascular disease as well as for an increased cardiovascular mortality. Xanthine oxidase is a critical source of reactive oxygen species contributing to vascular inflammation and endothelial dysfunction. Although a causal relationship between these conditions has not been clearly clarified, the capacity of uric acid to negatively affect vascular function by pro-oxidant effects and by decreasing nitric oxide bioavailability and consequently induce endothelial dysfunction may explain the association among hyperuricemia, hypertension, metabolic syndrome, and cardiovascular disease, also by a common mechanicistic point of view.
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