Uric acid transport and disease

被引:693
|
作者
So, Alexander [3 ]
Thorens, Bernard [1 ,2 ]
机构
[1] Univ Lausanne, Ctr Integrat Genom, CH-1015 Lausanne, Switzerland
[2] Univ Lausanne, Dept Physiol, CH-1015 Lausanne, Switzerland
[3] Univ Lausanne, Dept Musculoskeletal Med, Serv Rhumatol, CH-1015 Lausanne, Switzerland
来源
JOURNAL OF CLINICAL INVESTIGATION | 2010年 / 120卷 / 06期
基金
瑞士国家科学基金会;
关键词
ORGANIC ANION TRANSPORTER; NITRIC-OXIDE SYNTHASE; URATE EFFLUX TRANSPORTER; CORONARY-ARTERY-DISEASE; GENOME-WIDE ASSOCIATION; INSULIN-RESISTANCE; RENAL HYPOURICEMIA; CARDIOVASCULAR-DISEASE; METABOLIC SYNDROME; ENDOTHELIAL DYSFUNCTION;
D O I
10.1172/JCI42344
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Uric acid is the metabolic end product of purine metabolism in humans. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironrnent. Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. We discuss here the biology of urate metabolism and its role in disease. We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.
引用
收藏
页码:1791 / 1799
页数:9
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