Molecular physiology of urate transport

被引:265
作者
Hediger, MA
Johnson, RJ
Miyazaki, H
Endou, H
机构
[1] Brigham & Womens Hosp, Membrane Biol Program, Boston, MA 02115 USA
[2] Brigham & Womens Hosp, Div Renal, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Boston, MA 02115 USA
[4] Univ Florida, Div Nephrol Hypertens & Transplantat, Gainesville, FL USA
[5] Kumamoto Univ, Grad Sch Med Sci, Dept Nephrol, Kumamoto, Japan
[6] Kyorin Univ, Sch Med, Dept Pharmacol & Toxicol, Tokyo, Japan
关键词
D O I
10.1152/physiol.00039.2004
中图分类号
Q4 [生理学];
学科分类号
071003 [生理学];
摘要
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.
引用
收藏
页码:125 / 133
页数:9
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