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

doi:10.16352/j.issn.1001-6325.2023.09.1467

Abstract

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

CLC Number:

R589.7

YANG Lijuan, DONG Qiumei, WU Hao. Progress on the role of ABCG2 and SLC2A9 in the onset of hyperuricemia and gout[J]. Basic & Clinical Medicine, 2023, 43(9): 1467-1471.

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URL: http://journal11.magtechjournal.com/Jwk_jcyxylc/EN/10.16352/j.issn.1001-6325.2023.09.1467

http://journal11.magtechjournal.com/Jwk_jcyxylc/EN/Y2023/V43/I9/1467

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