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Review
. 2017 Aug 10;8(59):100852-100862.
doi: 10.18632/oncotarget.20135. eCollection 2017 Nov 21.

Recent advances on uric acid transporters

Liuqing Xu  1 , Yingfeng Shi  1 , Shougang Zhuang  1   2 , Na Liu  1
Affiliations
Review

Recent advances on uric acid transporters

Liuqing Xu et al. Oncotarget. .

Abstract

Uric acid is the product of purine metabolism and its increased levels result in hyperuricemia. A number of epidemiological reports link hyperuricemia with multiple disorders, such as kidney diseases, cardiovascular diseases and diabetes. Recent studies also showed that expression and functional changes of urate transporters are associated with hyperuricemia. Uric acid transporters are divided into two categories: urate reabsorption transporters, including urate anion transporter 1 (URAT1), organic anion transporter 4 (OAT4) and glucose transporter 9 (GLUT9), and urate excretion transporetrs, including OAT1, OAT3, urate transporter (UAT), multidrug resistance protein 4 (MRP4/ABCC4), ABCG-2 and sodium-dependent phosphate transport protein. In the kidney, uric acid transporters decrease the reabsorption of urate and increase its secretion. These transporters' dysfunction would lead to hyperuricemia. As the function of urate transporters is important to control the level of serum uric acid, studies on the functional role of uric acid transporter may provide a new strategy to treat hyperuricemia associated diseases, such as gout, chronic kidney disease, hyperlipidemia, hypertension, coronary heart disease, diabetes and other disorders. This review article summarizes the physiology of urate reabsorption and excretion transporters and highlights the recent advances on their roles in hyperuricemia and various diseases.

Keywords: hyperuricemia; structure and function; uric acid transporter protein.

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Conflict of interest statement

CONFLICTS OF INTEREST No authors have any competing interests.

Figures

Figure 1
Figure 1. Uric acid transports in kidney epithelial cells
The urate reabsorption pathway involves the apical exchanger proteins URAT1 and OAT4; intracellular urate is excreted through basolateral GLUT9L. Some uric acid excretion agents such as probenecid, sulfinpyrazone, benzbromarone and NSAIDs promote the excretion uric acid by combining with URAT1 to interrupt the reabsorption of uric acid. The excretion pathway critically involves the basolateral exchanger proteins OAT1 and OAT3, and the apical ATP-binding cassette proteins MRP4 and ABCG2.
See this image and copyright information in PMC

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