Reviews:
Recent advances on uric acid transporters
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Abstract
Liuqing Xu1, Yingfeng Shi1, Shougang Zhuang1,2 and Na Liu1
1Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
2Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI 02903, USA
Correspondence to:
Na Liu, email: [email protected]
Keywords: hyperuricemia, uric acid transporter protein, structure and function
Received: May 30, 2017 Accepted: July 29, 2017 Published: August 10, 2017
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.
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