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Effects of multiple genetic loci on the pathogenesis from serum urate to gout.
Sci Rep. 2017 03 02; 7:43614.SR

Abstract

Gout is a common arthritis resulting from increased serum urate, and many loci have been identified that are associated with serum urate and gout. However, their influence on the progression from elevated serum urate levels to gout is unclear. This study aims to explore systematically the effects of genetic variants on the pathogenesis in approximately 5,000 Chinese individuals. Six genes (PDZK1, GCKR, TRIM46, HNF4G, SLC17A1, LRRC16A) were determined to be associated with serum urate (PFDR < 0.05) in the Chinese population for the first time. ABCG2 and a novel gene, SLC17A4, contributed to the development of gout from hyperuricemia (OR = 1.56, PFDR = 3.68E-09; OR = 1.27, PFDR = 0.013, respectively). Also, HNF4G is a novel gene associated with susceptibility to gout (OR = 1.28, PFDR = 1.08E-03). In addition, A1CF and TRIM46 were identified as associated with gout in the Chinese population for the first time (PFDR < 0.05). The present study systematically determined genetic effects on the progression from elevated serum urate to gout and suggests that urate-associated genes functioning as urate transporters may play a specific role in the pathogenesis of gout. Furthermore, two novel gout-associated genes (HNF4G and SLC17A4) were identified.

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Authors+Show Affiliations

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China.

Division of Rheumatology and Immunology, Changhai Hospital, Shanghai, China.

Division of Rheumatology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China.

Division of Rheumatology, Taixing People's Hospital, Jiangsu Province, China.

Division of Rheumatology, Taizhou People's Hospital, Jiangsu Province, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China. Fudan-Taizhou Institute of Health Sciences, Taizhou, Jiangsu Province, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China. Fudan-Taizhou Institute of Health Sciences, Taizhou, Jiangsu Province, China.

Division of Rheumatology and Immunology, Changhai Hospital, Shanghai, China.

Division of Rheumatology and Immunology, Changhai Hospital, Shanghai, China.

Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China. Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China. Fudan-Taizhou Institute of Health Sciences, Taizhou, Jiangsu Province, China.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Jiangwan Campus, Shanghai, China. Fudan-Taizhou Institute of Health Sciences, Taizhou, Jiangsu Province, China. Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai, China.

MeSH

AllelesCase-Control StudiesDisease ProgressionFemaleGene ExpressionGenetic Association StudiesGenetic LociGenetic Predisposition to DiseaseGenotypeGoutHumansHyperuricemiaMalePolymorphism, Single NucleotideRisk FactorsSex FactorsUric Acid

Pub Type(s)

Journal Article

Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28252667

Citation

Dong, Zheng, et al. "Effects of Multiple Genetic Loci On the Pathogenesis From Serum Urate to Gout." Scientific Reports, vol. 7, 2017, p. 43614.

Dong Z, Zhou J, Jiang S, et al. Effects of multiple genetic loci on the pathogenesis from serum urate to gout. Sci Rep. 2017;7:43614.

Dong, Z., Zhou, J., Jiang, S., Li, Y., Zhao, D., Yang, C., Ma, Y., Wang, Y., He, H., Ji, H., Yang, Y., Wang, X., Xu, X., Pang, Y., Zou, H., Jin, L., & Wang, J. (2017). Effects of multiple genetic loci on the pathogenesis from serum urate to gout. Scientific Reports, 7, 43614. https://doi.org/10.1038/srep43614

Dong Z, et al. Effects of Multiple Genetic Loci On the Pathogenesis From Serum Urate to Gout. Sci Rep. 2017 03 2;7:43614. PubMed PMID: 28252667.

* Article titles in AMA citation format should be in sentence-case

TY - JOUR T1 - Effects of multiple genetic loci on the pathogenesis from serum urate to gout. AU - Dong,Zheng, AU - Zhou,Jingru, AU - Jiang,Shuai, AU - Li,Yuan, AU - Zhao,Dongbao, AU - Yang,Chengde, AU - Ma,Yanyun, AU - Wang,Yi, AU - He,Hongjun, AU - Ji,Hengdong, AU - Yang,Yajun, AU - Wang,Xiaofeng, AU - Xu,Xia, AU - Pang,Yafei, AU - Zou,Hejian, AU - Jin,Li, AU - Wang,Jiucun, Y1 - 2017/03/02/ PY - 2016/06/14/received PY - 2017/01/26/accepted PY - 2017/3/3/entrez PY - 2017/3/3/pubmed PY - 2018/11/9/medline SP - 43614 EP - 43614 JF - Scientific reports JO - Sci Rep VL - 7 N2 - Gout is a common arthritis resulting from increased serum urate, and many loci have been identified that are associated with serum urate and gout. However, their influence on the progression from elevated serum urate levels to gout is unclear. This study aims to explore systematically the effects of genetic variants on the pathogenesis in approximately 5,000 Chinese individuals. Six genes (PDZK1, GCKR, TRIM46, HNF4G, SLC17A1, LRRC16A) were determined to be associated with serum urate (PFDR < 0.05) in the Chinese population for the first time. ABCG2 and a novel gene, SLC17A4, contributed to the development of gout from hyperuricemia (OR = 1.56, PFDR = 3.68E-09; OR = 1.27, PFDR = 0.013, respectively). Also, HNF4G is a novel gene associated with susceptibility to gout (OR = 1.28, PFDR = 1.08E-03). In addition, A1CF and TRIM46 were identified as associated with gout in the Chinese population for the first time (PFDR < 0.05). The present study systematically determined genetic effects on the progression from elevated serum urate to gout and suggests that urate-associated genes functioning as urate transporters may play a specific role in the pathogenesis of gout. Furthermore, two novel gout-associated genes (HNF4G and SLC17A4) were identified. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/28252667/Effects_of_multiple_genetic_loci_on_the_pathogenesis_from_serum_urate_to_gout_ DB - PRIME DP - Unbound Medicine ER -