期刊
SEMINARS IN NEPHROLOGY
卷 31, 期 5, 页码 400-409出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2011.08.003
关键词
Hypouricemia; hyperuricemia; gout; genome-wide association study; diuretics
资金
- Japan Society for the Promotion of Science (JSPS) [KAKENHI 21390073, 21659216]
- Takeda Science Foundation
- Gout Research Foundation of Japan
- Nakatomi Foundation
- Grants-in-Aid for Scientific Research [21390073, 21659216] Funding Source: KAKEN
Urate (uric acid) is the end product of purine metabolism in human beings owing to the genetic loss of hepatic urate oxidase (uricase). Despite its potential advantage as an antioxidant, sustained hyperuricemia is associated with gout, renal diseases, hypertension, and cardiovascular diseases. Because the kidney plays a dominant role in maintaining serum urate levels through its excretion, it is important to understand the molecular mechanism of renal urate handling. Although molecular identification of the urate/anion exchanger URAT1 (SLC22A12) in 2002 paved the way for successive identification of several urate transport related proteins, the entire picture of effective renal urate handling in human beings has not yet been clarified. Recently, several genome-wide association studies have revealed close associations between serum urate levels and single nucleotide polymorphisms in at least 10 genetic loci including eight transporter-related genes. These findings led us to consider the roles of urate transporters in extrarenal tissues such as the intestine. In this review, we discuss various aspects of transmembrane transport of urate in the human body. Semin Nephrol 31:400-409 (C) 2011 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据