Molecular physiology of urate transport.
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.
Hediger
Matthias A
MA
Membrane Biology Program and Renal Division, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. mhediger@rics.bwh.harvard.edu
Johnson
Richard J
RJ
Miyazaki
Hiroki
H
Endou
Hitoshi
H
D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism; D007669:Kidney Calculi / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D027361:Organic Anion Transporters / Q000378:metabolism*; D014527:Uric Acid / Q000378:metabolism*
D027361:Organic Anion Transporters; C103862:urate transporter; D014527:Uric Acid