Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Humans excrete uric acid as the final breakdown product of unwanted purine nucleotides. Urate scavenges potential harmful radicals in our body. However, in conjunction with genetic or environmental (especially dietary) factors, urate may cause gout, nephrolitiasis, hypertension, and vascular disease. Blood levels of urate are maintained by the balance between generation and excretion. Excretion requires specialized transporters located in renal proximal tubule cells, intestinal epithelial cells, and vascular smooth muscle cells. The recently identified human urate transporters URAT1, MRP4, OAT1, and OAT3 are thought to play central roles in homeostasis and may prove interesting targets for future drug development.
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PMID:Molecular physiology of urate transport. 1577 1

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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PMID:Recent advances on uric acid transporters. 2924 27

The abnormal metabolism of uric acid results in many disease such as chronic kidney disease, hyperuricemia, nephrolithiasis, gout, hypertension, vascular disease and so on. Serum uric acid levels are maintained by the balance between production and elimination. There are many factors that maintain the balance of serum uric acid. One of them is transporters which are responsible for the debouchment of uric acid within blood. The transport and excretion of uric acid is a complicated procedure which is related with various transporters such as OAT1, OAT3, OAT4, URAT1, GLUT9, BCRP, MRP4, NPT1, NTP4, and so on. In recent years, a large number of genome-wide association studies have shown that the single nucleotide polymorphisms of uric acid transporters were closely related to serum uric acid level. What's more, some mutations on these gene locus may also break the balance of serum uric acid. Here, the polymorphisms of uric acid transporters closely related with the serum uric acid balance were reviewed and discussed because of their important significance in clinical therapy for a precision medicine. The mechanism of metabolic diseases with gene variation may provide new strategy for the design and development of innovative drug to treat diseases with uric acid metabolic disturbance.
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PMID:The effect of polymorphism of uric acid transporters on uric acid transport. 3038 60