基础医学与临床 ›› 2023, Vol. 43 ›› Issue (9): 1467-1471.doi: 10.16352/j.issn.1001-6325.2023.09.1467

• 短篇综述 • 上一篇    下一篇

ABCG2SLC2A9在高尿酸血症和痛风发病中作用的研究进展

杨丽娟1,2, 董秋梅1*, 吴昊1   

  1. 1.内蒙古医科大学,内蒙古 呼和浩特 010107;
    2.内蒙古自治区中医医院,内蒙古 呼和浩特 010020
  • 收稿日期:2022-08-08 修回日期:2023-02-27 出版日期:2023-09-05 发布日期:2023-09-01
  • 通讯作者: *d.qium@163.com
  • 基金资助:
    内蒙古自治区科技计划(2020GG0194)

Progress on the role of ABCG2 and SLC2A9 in the onset of hyperuricemia and gout

YANG Lijuan1,2, DONG Qiumei1*, WU Hao1   

  1. 1. Inner Mongolia Medical University, Hohhot 010107;
    2. Inner Mongolia Autonomous Region Hospital of Traditional Chinese Medicine,Hohhot 010020, China
  • Received:2022-08-08 Revised:2023-02-27 Online:2023-09-05 Published:2023-09-01
  • Contact: *d.qium@163.com

摘要: ABCG2SLC2A9编码尿酸转运蛋白ABCG2和GLUT9。ABCG2单核苷酸多态性(SNP)可以使ABCG2蛋白表达减少、转运功能下降,继而引发肠道尿酸排泄功能障碍,导致血尿酸升高。SLC2A9对血尿酸的调节较为复杂,该基因功能缺失会引起肾小管尿酸重吸收减少、肠道尿酸排泄障碍和肝脏摄取尿酸障碍。ABCG2通过引起高尿酸血症(HUA)和增加炎性反应促进痛风发作。SLC2A9功能缺失反而可以减轻氧化和炎性反应。此外,ABCG2与早发痛风有着密切关系,其SNP是早发痛风的危险因素。

关键词: ABCG2, SLC2A9, 高尿酸血症, 痛风

Abstract: ABCG2 and SLC2A9 encode the uric acid transporters ABCG2 and GLUT9. ABCG2 single nucleotide polymorphism (SNP) can reduce the expression and transport function of ABCG2 protein, and then cause intestinal uric acid excretion dysfunction, resulting in the increase of blood uric acid. The regulation of blood uric acid by SLC2A9 is complicated. Loss of function of SLC2A9 may lead to decreased renal tubule uric acid reabsorption, impaired intestinal uric acid excretion and impaired hepatic uric acid uptake. ABCG2 promotes gout attacks by causing hyperuricemia(HUA) and increasing inflammatory responses. On the contray, loss of function of SLC2A9 can instead reduce oxidation and inflammatory responses. In addition, ABCG2 has a close relationship with early-onset gout and its SNP is a risk factor for early onset gout.

Key words: ABCG2, SLC2A9, hyperuricemia, gout

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