Rizzo Manfredi, Obradovic Milan, Labudovic-Borovic Milica, Nikolic Dragana, Montalto Giuseppe, Rizvi Ali A, Mikhailidis Dimitri P, Isenovic Esma R
Institute Vinca, University of Belgrade, Laboratory of Radiobiology and Molecular Genetics, P.O. Box 522, 11000 Belgrade, Serbia.
Curr Vasc Pharmacol. 2014;12(4):572-85. doi: 10.2174/1570161111999131205160756.
In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.
在人类中,尿酸(UA)是嘌呤降解的终产物。肾脏系统对尿酸的处理是一个复杂的过程,目前尚未完全了解。迄今为止,已在肾近端小管中鉴定出几种尿酸转运蛋白。其中,尿酸转运蛋白1(URAT1)和葡萄糖转运蛋白9(GLUT9)被认为更为重要,它们是治疗高尿酸血症及潜在相关心血管代谢风险的潜在靶点。因此,认识尿酸的代谢途径并阐明高尿酸血症的发生情况,可能为了解尿酸、高血压前期(preHT)和代谢综合征(MetS)之间的关系提供重要线索。我们还综述了该领域现有的临床研究,包括探讨尿酸通过不同转运蛋白转运机制的实验研究,以及针对患有MetS、preHT或心血管危险因素的高尿酸血症患者的当前治疗选择。