Ontology type: schema:ScholarlyArticle Open Access: True
2015-05-13
AUTHORSChanggui Li, Zhiqiang Li, Shiguo Liu, Can Wang, Lin Han, Lingling Cui, Jingguo Zhou, Hejian Zou, Zhen Liu, Jianhua Chen, Xiaoyu Cheng, Zhaowei Zhou, Chengcheng Ding, Meng Wang, Tong Chen, Ying Cui, Hongmei He, Keke Zhang, Congcong Yin, Yunlong Wang, Shichao Xing, Baojie Li, Jue Ji, Zhaotong Jia, Lidan Ma, Jiapeng Niu, Ying Xin, Tian Liu, Nan Chu, Qing Yu, Wei Ren, Xuefeng Wang, Aiqing Zhang, Yuping Sun, Haili Wang, Jie Lu, Yuanyuan Li, Yufeng Qing, Gang Chen, Yangang Wang, Li Zhou, Haitao Niu, Jun Liang, Qian Dong, Xinde Li, Qing-Sheng Mi, Yongyong Shi
ABSTRACTGout is one of the most common types of inflammatory arthritis, caused by the deposition of monosodium urate crystals in and around the joints. Previous genome-wide association studies (GWASs) have identified many genetic loci associated with raised serum urate concentrations. However, hyperuricemia alone is not sufficient for the development of gout arthritis. Here we conduct a multistage GWAS in Han Chinese using 4,275 male gout patients and 6,272 normal male controls (1,255 cases and 1,848 controls were genome-wide genotyped), with an additional 1,644 hyperuricemic controls. We discover three new risk loci, 17q23.2 (rs11653176, P=1.36 × 10−13, BCAS3), 9p24.2 (rs12236871, P=1.48 × 10−10, RFX3) and 11p15.5 (rs179785, P=1.28 × 10−8, KCNQ1), which contain inflammatory candidate genes. Our results suggest that these loci are most likely related to the progression from hyperuricemia to inflammatory gout, which will provide new insights into the pathogenesis of gout arthritis. More... »
PAGES7041
http://scigraph.springernature.com/pub.10.1038/ncomms8041
DOIhttp://dx.doi.org/10.1038/ncomms8041
DIMENSIONShttps://app.dimensions.ai/details/publication/pub.1031524864
PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/25967671
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