中国全科医学 ›› 2023, Vol. 26 ›› Issue (15): 1916-1922.DOI: 10.12114/j.issn.1007-9572.2022.0747

• 综述与专论 • 上一篇    下一篇

尿酸排泄及其相关转运蛋白在高尿酸血症中的研究进展

辛家东1,2,3,4, 周嘉宝1,2,3,4, 吴志远1,2,3,4, 张栩铭1,2,3,4, 高建东1,2,3,4,*()   

  1. 1.200120 上海市,上海中医药大学附属曙光医院肾病科
    2.200000 上海市,上海中医药大学中医肾病研究所
    3.200000 上海市,肝肾疾病病证教育部重点实验室
    4.201203 上海市中医临床重点实验室
  • 收稿日期:2022-10-12 修回日期:2022-12-16 出版日期:2023-05-20 发布日期:2022-12-22
  • 通讯作者: 高建东

  • 作者贡献:辛家东提出研究选题方向及撰写论文初稿;周嘉宝负责相关内容的文献收集和整理;吴志远负责论文的修订;张栩铭负责文章的质量控制及审校;高建东对文章整体负责;所有作者确认了论文的最终稿。
  • 基金资助:
    国家自然科学基金资助项目(81874437); 国家自然科学基金青年项目(81904126); 上海市科委项目(20Y21901800)

Advances in Urate Excretion and Urate Transporters in Hyperuricemia

XIN Jiadong1,2,3,4, ZHOU Jiabao1,2,3,4, WU Zhiyuan1,2,3,4, ZHANG Xuming1,2,3,4, GAO Jiandong1,2,3,4,*()   

  1. 1. Department of Nephrology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine1, Shanghai 200120, China
    2. TCM Institute of Kidney Disease, Shanghai University of Traditional Chinese Medicine, Shanghai 200000, China
    3. Key Laboratory of Liver and Kidney Diseases, Ministry of Education, Shanghai 200000, China
    4. Shanghai Key Laboratory of Traditional Chinese Clinical Medicine, Shanghai 201203, China
  • Received:2022-10-12 Revised:2022-12-16 Published:2023-05-20 Online:2022-12-22
  • Contact: GAO Jiandong

摘要: 高尿酸血症(HUA)是人体内尿酸生成和排泄稳态失调从而导致血清尿酸水平升高超过参考范围的一类异质性疾病。既往研究发现3个常见尿酸转运蛋白基因(ABCG2、SLC2A9和SLC22A12)对人体血清尿酸水平的影响程度较大,其他尿酸相关的转运蛋白基因(如SLC16A9、SLC22A6、SLC22A7、SLC22A8、SLC22A9、SLC22A11、SLC22A13和ABCC4等)也对尿酸水平的调节起着至关重要的作用。本文对上述已发现的与HUA发生和发展相关的尿酸转运蛋白做一综述,主要包括肾脏中的尿酸重吸收转运蛋白和尿酸分泌转运蛋白以及肠道中的尿酸转运蛋白,旨在为今后HUA的临床治疗提供理论和数据支持。

关键词: 高尿酸血症, 尿酸, 尿酸转运蛋白, 基因表达, 综述

Abstract:

Hyperuricemia is a heterogeneous disease caused by dysregulation of the homeostasis of urate production and excretion, which leads to the elevation of blood uric acid beyond the normal range. It has been found that three common genes ABCG2, SLC2A9 and SLC22A12 have a great influence on serum uric acid level in human body. Other urate transporter genes, such as SLC16A9, SLC22A6, SLC22A7, SLC22A8, SLC22A9, SLC22A11, SLC22A13 and ABCC4 also play a crucial role in the regulation of urate levels. This article reviews the urate transporters mentioned above that have been found to be related to the development of hyperuricemia, including uric acid reabsorption transporter and uric acid secretion transporter in kidney, uric acid transporter in intestine, aiming at providing theoretical and data support for future clinical treatment.

Key words: Hyperuricemia, Uric acid, Uric acid transporter, Gene expression, Review