ISSN 1006-298X      CN 32-1425/R

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肾脏病与透析肾移植杂志 ›› 2014, Vol. 23 ›› Issue (5): 467-471.

• 论文 • 上一篇    下一篇

肾脏调节尿酸排泄的分子机制

  

  • 出版日期:2014-10-28 发布日期:2014-11-03

Molecular mechanisms in the regulation of uric acid excretion

  • Online:2014-10-28 Published:2014-11-03

摘要:

摘要 痛风是由于长期嘌呤代谢紊乱所导致的一种炎症性关节炎,高尿酸血症是其发病的重要生物化学基础。全基因组关联研究(genome-wide association studies, GWAS)以及meta分析等研究发现了许多导致高尿酸血症的基因,其中研究较为充分的包括SLC2A9、ABCG2以及SLC22A12。SLC2A9基因编码GLUT-9,GLUT-9参与调节肾小管转运尿酸,在近端小管尿酸盐的重吸收中起到重要的作用。ABCG2编码ABCG2蛋白,在尿酸盐的顶端分泌中发挥着作用。SLC22A12基因编码URAT1,负责尿酸盐的重吸收。本文通过阐述这三个基因以及其他一些基因与高尿酸血症的关系来探究肾脏调节尿酸排泄的分子机制。

关键词: 高尿酸血症, 基因组, 分子机制

Abstract:

ABSTRACT Gout is a kind of inflammatory arthritis resulted from long term purine metabolic disturbance, with hyperuricaemia as its key biochemical basis. The genome-wide association studies (GWAS) and meta analysis have found many genes which are relevant with hyperuricaemia. Three of these genes have been studied sufficiently, including SLC2A9, ABCG2, and SLC22A12. SLC2A9 encodes GLUT-9, which participates in the regulation of uric acid reabsorption at the proximal tubule. ABCG2 protein plays a role in the process of the apical secretion of urate. SLC22A12 encodes URAT1, which is also responsible for the reabsorption of urate. In this paper, through discussing the relationship between these genes and hyperuricaemia, the molecular mechanisms about the regulation of uric acid excretion will be investigated.

Key words: hyperuricaemia, genome, molecular mechanisms