1 Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Nanchang University, Nanchang, China
2 Department of Internal Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA
3 Department of Ophthalmology of Children, The Second Affiliated Hospital of Nanchang University, Nanchang, China
Gout is a common form of inflammatory arthritis caused by hyperuricemia and the deposition of Monosodium Urate (MSU) crystals. It is also considered as a complex disorder in which multiple genetic factors have been identified in association with its susceptibility and/or clinical outcomes. Major genes that were associated with gout include URAT1, GLUT9, OAT4, NPT1 (SLC17A1), NPT4 (SLC17A3), NPT5 (SLC17A4), MCT9, ABCG2, ABCC4, KCNQ1, PDZK1, NIPAL1, IL1β, IL-8, IL-12B, IL-23R, TNFA, MCP-1/CCL2, NLRP3, PPARGC1B, TLR4, CD14, CARD8, P2X7R, EGF, A1CF, HNF4G and TRIM46, LRP2, GKRP, ADRB3, ADH1B, ALDH2, COMT, MAOA, PRKG2, WDR1, ALPK1, CARMIL (LRRC16A), RFX3, BCAS3, CNIH-2, FAM35A and MYL2-CUX2. The proteins encoded by these genes mainly function in urate transport, inflammation, innate immunity and metabolism. Understanding the functions of gout-associated genes will provide important insights into future studies to explore the pathogenesis of gout, as well as to develop targeted therapies for gout.
Keywords: Gout, Single nucleotide polymorphism, Genome-wide association study, Case-control study, Imume regulatory genes, MSU.
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* Address correspondence to this author at the Department of Internal Medicine/Rheumatology, University of Texas Health Science Center at Houston McGovern Medical School, Houston, TX, USA; Tel: 713-500-6088; E-mail: email@example.com