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心血管损伤的尿酸相关机制新见解

New Insight into Urate-Related Mechanism of Cardiovascular Damage.

作者信息

Grassi Davide, Desideri Giovambattista, Ferri Claudio

机构信息

University of L'Aquila, Department of Life, Health, and Environmental Sciences, Viale S Salvatore, Delta, 6 Medicina, 67100 Coppito, L'Aquila, Italy.

出版信息

Curr Pharm Des. 2014;20(39):6089-95. doi: 10.2174/1381612820666140417095730.

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.

摘要

多项实验和临床研究报告称,高尿酸血症可能引发高血压、代谢综合征、血管损伤和肾脏疾病。此外,相当一部分流行病学研究与以下假设相符:高尿酸血症可能是心血管疾病以及心血管死亡率增加的独立危险因素。黄嘌呤氧化酶是活性氧的关键来源,会导致血管炎症和内皮功能障碍。尽管这些情况之间的因果关系尚未明确,但尿酸通过促氧化作用以及降低一氧化氮生物利用度进而诱导内皮功能障碍,对血管功能产生负面影响的能力,也可以从共同的机制角度解释高尿酸血症、高血压、代谢综合征和心血管疾病之间的关联。

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