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Coronary Artery Disease: HELP
Articles by Fan Wang
Based on 19 articles published since 2010
(Why 19 articles?)
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Between 2010 and 2020, Fan Wang wrote the following 19 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Article Long noncoding RNA 2019

Cho, Hyosuk / Shen, Gong-Qing / Wang, Xiaofeng / Wang, Fan / Archacki, Stephen / Li, Yabo / Yu, Gang / Chakrabarti, Susmita / Chen, Qiuyun / Wang, Qing Kenneth. ·From the Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, Ohio 44106. · the Departments of Cardiovascular and Metabolic Sciences and. · the Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio 44195, and. · Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195. · the Key Laboratory of Molecular Biophysics of the Ministry of Education, Cardio-X Center, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan 430073, China. · the Departments of Cardiovascular and Metabolic Sciences and chenq3@ccf.org. · From the Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, Ohio 44106, wangq2@ccf.org. ·J Biol Chem · Pubmed #30655286.

ABSTRACT: Coronary artery disease (CAD) is the leading cause of death worldwide. Long noncoding RNAs (lncRNAs) are a class of noncoding transcripts of > 200 nucleotides and are increasingly recognized as playing functional roles in physiology and disease.

2 Article Genetic Regulation of the Thymic Stromal Lymphopoietin (TSLP)/TSLP Receptor (TSLPR) Gene Expression and Influence of Epistatic Interactions Between IL-33 and the TSLP/TSLPR Axis on Risk of Coronary Artery Disease. 2018

Nie, Shao-Fang / Zha, Ling-Feng / Fan, Qian / Liao, Yu-Hua / Zhang, Hong-Song / Chen, Qian-Wen / Wang, Fan / Tang, Ting-Ting / Xia, Ni / Xu, Cheng-Qi / Zhang, Jiao-Yue / Lu, Yu-Zhi / Zeng, Zhi-Peng / Jiao, Jiao / Li, Yuan-Yuan / Xie, Tian / Zhang, Wen-Juan / Wang, Dan / Wang, Chu-Chu / Fa, Jing-Jing / Xiong, Hong-Bo / Ye, Jian / Yang, Qing / Wang, Peng-Yun / Tian, Sheng-Hua / Lv, Qiu-Lun / Li, Qing-Xian / Qian, Jin / Li, Bin / Wu, Gang / Wu, Yan-Xia / Yang, Yan / Yang, Xiang-Ping / Hu, Yu / Wang, Qing K / Cheng, Xiang / Tu, Xin. ·Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Key Laboratory for Biological Targeted Therapy of Education Ministry and Hubei Province, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Innovation Institute, Huazhong University of Science and Technology, Wuhan, China. · Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, China. · Department of Molecular Cardiology, Cleveland Clinic Lerner Research Institute, Cleveland, OH, United States. · Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, China. · Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Department of Geriatrics, the Central Hospital of Wuhan, Tongji Medica College, Huazhong University of Science and Technology, Wuhan, China. · Section of Molecule Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States. · Jining Medical College Affiliated Hospital, Jining, China. · Suizhou Central Hospital, Suizhou, China. · Xiangyang Central Hospital, Xiangyang, China. · Renmin Hospital of Wuhan University, Wuhan, China. · Wuhan No. 1 Hospital, Wuhan, China. · School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. ·Front Immunol · Pubmed #30123216.

ABSTRACT: The thymic stromal lymphopoietin (TSLP)/TSLP receptor (TSLPR) axis is involved in multiple inflammatory immune diseases, including coronary artery disease (CAD). To explore the causal relationship between this axis and CAD, we performed a three-stage case-control association analysis with 3,628 CAD cases and 3,776 controls using common variants in the genes

3 Article Analysis of causal effect of APOA5 variants on premature coronary artery disease. 2018

Wang, Fan / Wang, Isabel Z / Ellis, Stephen / Archacki, Stephen / Barnard, John / Hubbard, Carlos / Topol, Eric J / Chen, Qiuyun / Wang, Qing K. ·Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA. · Department of Molecular Medicine, Department of Genetics and Genome Science, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, USA. · Shaker Heights High School, Shaker Heights, OH, USA. · Department of Cardiovascular Medicine, Sydell & Arnold Miller Family Heart & Vascular Institute, Cleveland Clinic, Cleveland, OH, USA. · Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA. · Scripps Translational Science Institute, Scripps Research Institute, Scripps Clinic, La Jolla, CA, USA. · The Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, P. R. China. ·Ann Hum Genet · Pubmed #30024021.

ABSTRACT: Apolipoprotein A5 (APOA5) regulates the metabolisms of triglyceride and HDL. APOA5 variants have been linked to coronary artery disease (CAD), but their causal roles are not well studied yet. This study aims to identify the causal effects of APOA5 variants on premature CAD. Sequencing analysis of APOA5 in 128 premature, familiar CAD patients from GeneQuest identified 11 genomic variants, including p.S19W (rs3135506). SKAT analysis showed that all sequenced variants, in aggregate, significantly increased the risk of premature CAD (P-skat = 0.037). Individually, the p.S19W variant was significantly associated with risk of premature CAD (OR = 2.30, P = 0.008) in an independent set of 342 premature CAD patients and 537 controls after adjusting for covariates of sex, age, hypertension, body mass index, triglycerides (TGs), and total, LDL-, and HDL-cholesterol levels. Meanwhile, p.S19W significantly correlated with HDL-C levels (P = 0.048) and TG levels (P = 0.025). Mediation analysis yielded a mediation effect of p.S19W on risk of premature CAD through HDL-C (OR = 0.98, P = 0.040) and TG (OR = 0.98, P = 0.042), suggesting a causal relationship between p.S19W and premature CAD partially through its effects on HDL-C and TG levels. These results suggest that APOA5 variation regulates TG and HDL levels, thus displaying a causal role in the development of CAD.

4 Article IL-13 may be involved in the development of CAD via different mechanisms under different conditions in a Chinese Han population. 2018

Zha, Ling-Feng / Nie, Shao-Fang / Chen, Qian-Wen / Liao, Yu-Hua / Zhang, Hong-Song / Dong, Jiang-Tao / Xie, Tian / Wang, Fan / Tang, Ting-Ting / Xia, Ni / Xu, Cheng-Qi / Zhou, Ying-Chao / Zeng, Zhi-Peng / Jiao, Jiao / Wang, Peng-Yun / Wang, Qing K / Tu, Xin / Cheng, Xiang. ·Department of cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. · Key Lab for biological targeted therapy of Education Ministry and Hubei province, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. · Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, PA, 19104, USA. · Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, 430074, China. · Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, 430074, China. xtu@hust.edu.cn. · Department of cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. nathancx@mail.hust.edu.cn. · Key Lab for biological targeted therapy of Education Ministry and Hubei province, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. nathancx@mail.hust.edu.cn. ·Sci Rep · Pubmed #29670225.

ABSTRACT: Interleukin-13 (IL-13) has important functions in atherosclerosis, but its role in coronary artery disease (CAD) is unclear. Here, we studied the genetic role of IL-13 in CAD in a Chinese Han population using tag SNPs covering the whole IL13 gene (i.e., rs1881457, rs2069744 and rs20541) and a two-stage cohort containing 1863 CAD cases and 1841 controls. Traditional risk factors for CAD, such as age, BMI, and other factors, were used as covariates in logistic regression analysis. In the total population, we found that two haplotypes of IL13 (ATG and ATA, ordered rs1881457

5 Article Genome-Wide Linkage Analysis of Large Multiple Multigenerational Families Identifies Novel Genetic Loci for Coronary Artery Disease. 2017

Guo, Yang / Wang, Fan / Li, Lin / Gao, Hanxiang / Arckacki, Stephen / Wang, Isabel Z / Barnard, John / Ellis, Stephen / Hubbard, Carlos / Topol, Eric J / Chen, Qiuyun / Wang, Qing K. ·Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. · Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, 44195, USA. · Heart Center, the First Affiliated Hospital, Lanzhou University, Lanzhou, Gansu, 730000, P. R. China. · Shaker Heights High School, Shaker Heights, OH, 44120, USA. · Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, 44195, USA. · Department of Cardiovascular Medicine, Sydell & Arnold Miller Family Heart & Vascular Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. · Scripps Translational Science Institute, Scripps Research Institute, Scripps Clinic, La Jolla, CA, 92037, USA. · Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. chenq3@ccf.org. · Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, 44195, USA. chenq3@ccf.org. · Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. wangq2@ccf.org. · Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, 44195, USA. wangq2@ccf.org. · Department of Cardiovascular Medicine, Sydell & Arnold Miller Family Heart & Vascular Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. wangq2@ccf.org. · Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA. wangq2@ccf.org. ·Sci Rep · Pubmed #28710368.

ABSTRACT: Coronary artery disease (CAD) is the leading cause of death, and genetic factors contribute significantly to risk of CAD. This study aims to identify new CAD genetic loci through a large-scale linkage analysis of 24 large and multigenerational families with 433 family members (GeneQuest II). All family members were genotyped with markers spaced by every 10 cM and a model-free nonparametric linkage (NPL-all) analysis was carried out. Two highly significant CAD loci were identified on chromosome 17q21.2 (NPL score of 6.20) and 7p22.2 (NPL score of 5.19). We also identified four loci with significant NPL scores between 4.09 and 4.99 on 2q33.3, 3q29, 5q13.2 and 9q22.33. Similar analyses in individual families confirmed the six significant CAD loci and identified seven new highly significant linkages on 9p24.2, 9q34.2, 12q13.13, 15q26.1, 17q22, 20p12.3, and 22q12.1, and two significant loci on 2q11.2 and 11q14.1. Two loci on 3q29 and 9q22.33 were also successfully replicated in our previous linkage analysis of 428 nuclear families. Moreover, two published risk variants, SNP rs46522 in UBE2Z and SNP rs6725887 in WDR12 by GWAS, were found within the 17q21.2 and 2q33.3 loci. These studies lay a foundation for future identification of causative variants and genes for CAD.

6 Article Identification of a molecular signaling gene-gene regulatory network between GWAS susceptibility genes ADTRP and MIA3/TANGO1 for coronary artery disease. 2017

Luo, Chunyan / Wang, Fan / Ren, Xiang / Ke, Tie / Xu, Chengqi / Tang, Bo / Qin, Subo / Yao, Yufeng / Chen, Qiuyun / Wang, Qing Kenneth. ·The Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan 430074, Hubei Province, PR China. · Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH 44195, USA; Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, OH 44195, USA. · Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH 44195, USA; Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, OH 44195, USA. Electronic address: chenq3@ccf.org. · The Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan 430074, Hubei Province, PR China; Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH 44195, USA; Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, OH 44195, USA. Electronic address: qkwang@hust.edu.cn. ·Biochim Biophys Acta Mol Basis Dis · Pubmed #28341552.

ABSTRACT: Coronary artery disease (CAD) is the leading cause of death worldwide. GWAS have identified >50 genomic loci for CAD, including ADTRP and MIA3/TANGO1. However, it is important to determine whether the GWAS genes form a molecular network. In this study, we have uncovered a novel molecular network between ADTRP and MIA3/TANGO1 for the pathogenesis of CAD. We showed that knockdown of ADTRP expression markedly down-regulated expression of MIA3/TANGO1. Mechanistically, ADTRP positively regulates expression of PIK3R3 encoding the regulatory subunit 3 of PI3K, which leads to activation of AKT, resulting in up-regulation of MIA3/TANGO1. Both ADTRP and MIA3/TANGO1 are involved in endothelial cell (EC) functions relevant to atherosclerosis. Knockdown of ADTRP expression by siRNA promoted oxidized-LDL-mediated monocyte adhesion to ECs and transendothelial migration of monocytes, inhibited EC proliferation and migration, and increased apoptosis, which was reversed by expression of constitutively active AKT1 and MIA3/TANGO1 overexpression, while the over-expression of ADTRP in ECs blunted these processes. Knockdown of MIA3/TANGO1 expression also promoted monocyte adhesion to ECs and transendothelial migration of monocytes, and vice versa for overexpression of MIA3/TANGO1. We found that ADTRP negatively regulates the levels of collagen VII and ApoB in HepG2 and endothelial cells, which are downstream regulatory targets of MIA3/TANGOI. In conclusion, we have uncovered a novel molecular signaling pathway for the pathogenesis of CAD, which involves a novel gene-gene regulatory network. We show that ADTRP positively regulates PIK3R3 expression, which leads to activation of AKT and up-regulation of MIA3/TANGO1, thereby regulating endothelial cell functions directly relevant to atherosclerosis.

7 Article Scavenger Receptor Class B Type 1 Deletion Led to Coronary Atherosclerosis and Ischemic Heart Disease in Low-density Lipoprotein Receptor Knockout Mice on Modified Western-type Diet. 2017

Liao, Jiawei / Guo, Xin / Wang, Mengyu / Dong, Chengyan / Gao, Mingming / Wang, Huan / Kayoumu, Abudurexiti / Shen, Qiang / Wang, Yuhui / Wang, Fan / Huang, Wei / Liu, George. ·Institute of Cardiovascular Sciences and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University Health Science Center. ·J Atheroscler Thromb · Pubmed #27373983.

ABSTRACT: AIM: Atherosclerosis-prone apolipoprotein E (apoE) or low-density lipoprotein receptor (LDL-R) knockout (KO) mice are generally resistant to developing coronary atherosclerosis (CA) and ischemic heart disease (IHD). However, studies have demonstrated the occurrence of spontaneous CA and IHD in scavenger receptor class B type 1 (SR-BI)/apoE double KO (dKO) mice, which suggests that SR-BI could be a potential target for the prevention and therapy of CA and IHD. This possibility was later investigated in SR-BI/LDL-R dKO mice, but no signs of CA or IHD was identified when mice were fed a normal western-type diet. Here we explored whether SR-BI deletion could result in CA and IHD in LDL-R KO mice when fed a modified western-type diet containing higher (0.5%) cholesterol. METHODS: Cardiac functions were detected by electrocardiography, single photon emission computed tomography (SPECT), echocardiography (Echo) and 2,3,5-triphenyltetrazolium chloride staining. CA was visualized by hematoxylin-eosin staining. RESULTS: After 12 weeks on the modified diet, SR-BI/LDL-R dKO mice developed cardiac ischemia/infarction, together with systolic dysfunction and left ventricular dilatation. CA was most severe at the aortic sinus level to an extent that no dKO mice survived to 20 weeks on the modified diet. None of control mice, however, developed CA or IHD. CONCLUSIONS: SR-BI deletion led to CA and IHD in LDL-R KO mice when fed the modified western-type diet. We established SR-BI/LDL-R dKO mice as a diet-induced murine model of human IHD and developed detection methods, using a combination of SPECT and Echo, for effective in vivo evaluation of cardiac functions.

8 Article Coronary artery disease susceptibility gene ADTRP regulates cell cycle progression, proliferation, and apoptosis by global gene expression regulation. 2016

Luo, Chunyan / Wang, Fan / Qin, Subo / Chen, Qiuyun / Wang, Qing K. ·The Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, People's Republic of China; · Department of Molecular Cardiology, Lerner Research Institute, Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio; and Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, Ohio qkwang@hust.edu.cn wangq2@ccf.org. · Department of Molecular Cardiology, Lerner Research Institute, Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio; and Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, Ohio. · The Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, People's Republic of China; Department of Molecular Cardiology, Lerner Research Institute, Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio; and Department of Molecular Medicine, Department of Genetics and Genome Science, Case Western Reserve University, Cleveland, Ohio. ·Physiol Genomics · Pubmed #27235449.

ABSTRACT: The ADTRP gene encodes the androgen-dependent TFPI-regulating protein and is a susceptibility gene for contrary artery disease (CAD). We performed global gene expression profiling for ADTRP knock-down using microarrays in human HepG2 cells. Follow-up real-time RT-PCR analysis demonstrated that ADTRP knock-down regulates a diverse set of genes, including upregulation of seven histone genes, downregulation of multiple cell cycle genes (CCND1, CDK4, and CDKN1A), and upregulation of apoptosis genes (CASP7 and PDCD2) in HepG2 cells and endothelial cells. Consistently, ADTRP increases the number of S phase cells during cell cycle, promotes cell proliferation, and inhibits apoptosis. Our study provides novel insights into the function of ADTRP and biological pathways involving ADTRP, which may be involved in the pathogenesis of CAD.

9 Article Analysis of the genetic association between IL27 variants and coronary artery disease in a Chinese Han population. 2016

Fan, Qian / Nie, Shaofang / Li, Sihui / Liao, Yuhua / Zhang, Hongsong / Zha, Lingfeng / Wang, Fan / Tang, Tingting / Xia, Ni / Xu, Chengqi / Wang, Pengyun / Xie, Tian / Xie, Jiangjiao / Lu, Qiulun / Li, Qingxian / Qian, Jin / Li, Bin / Wu, Gang / Wu, Yanxia / Yang, Yan / Wang, Qing K / Tu, Xin / Cheng, Xiang. ·Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, USA. · Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, China. · Section of Molecule Medicine, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, USA. · Department of Cardiology, Jining Medical College Affiliated Hospital, Jining, China. · Department of Cardiology, Suizhou Central Hospital, Suizhou, China. · Department of Cardiology, Xiangyang Central Hospital, Xiangyang, China. · Renmin Hospital of Wuhan University, Wuhan, China. · Wuhan No. 1 Hospital, Wuhan, China. ·Sci Rep · Pubmed #27174010.

ABSTRACT: Interleukin-27 (IL-27) is an important cytokine in inflammatory diseases, including coronary artery disease (CAD). To explore the precise role of IL-27 in CAD, we investigated the genetic association between IL27 and CAD in the GeneID Chinese Han population. A two-stage case control association analysis was performed for 3075 CAD cases and 2802 controls. Logistic regression analysis was used to adjust the traditional risk factors for CAD. Results showed that a promoter variant, rs153109, tended to be marginally associated with CAD in the discovery population (Padj = 0.028, OR = 1.27, 95%CI: 1.03-1.58). However, this association was not replicated in the validation stage (Padj = 0.559, OR = 1.04, 95%CI: 0.90-1.21). In addition, when we classified the combined population into two subgroups according to the age at disease onset or disease state, we again obtained no significant associations. Finally, we estimated the severity of coronary stenosis using the Gensini Scoring system and determined that the rs153109 genotypes were still not associated with the Gensini scores of the CAD patients. In conclusion, our study failed to find an association between common variants in the functional region of IL27 and CAD in a Chinese Han population, which indicated that IL-27 might only be an inflammatory marker during the development of CAD.

10 Article Genomic variant in CAV1 increases susceptibility to coronary artery disease and myocardial infarction. 2016

Chen, Shanshan / Wang, Xiaojing / Wang, Junhan / Zhao, Yuanyuan / Wang, Dan / Tan, Chengcheng / Fa, Jingjing / Zhang, Rongfeng / Wang, Fan / Xu, Chaoping / Huang, Yufeng / Li, Sisi / Yin, Dan / Xiong, Xin / Li, Xiuchun / Chen, Qiuyun / Tu, Xin / Yang, Yanzong / Xia, Yonglong / Xu, Chengqi / Wang, Qing K. ·Key Laboratory of Molecular Biophysics of the Ministry of Education, Cardio-X Institute, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, China. · Department of Clinical Laboratory, University Hospital, Huazhong University of Science and Technology, Wuhan, China. · Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, China. · Center for Cardiovascular Genetics, Department of Molecular Cardiology, Cleveland Clinic, and Department of Molecular Medicine, CCLCM, Case Western Reserve University, Cleveland, OH 44195, USA. ·Atherosclerosis · Pubmed #26775120.

ABSTRACT: BACKGROUND: The CAV1 gene encodes caveolin-1 expressed in cell types relevant to atherosclerosis. Cav-1-null mice showed a protective effect on atherosclerosis under the ApoE(-/-) background. However, it is unknown whether CAV1 is linked to CAD and MI in humans. In this study we analyzed a tagSNP for CAV1 in intron 2, rs3807989, for potential association with CAD. METHODS AND RESULTS: We performed case-control association studies in three independent Chinese Han populations from GeneID, including 1249 CAD cases and 841 controls in Population I, 1260 cases and 833 controls in Population II and 790 cases and 1212 controls in Population III (a total of 3299 cases and 2886 controls). We identified significant association between rs3807989 and CAD in three independent populations and in the combined population (Padj = 2.18 × 10(-5), OR = 1.19 for minor allele A). We also detected significant association between rs3807989 and MI (Padj = 5.43 × 10(-5), OR = 1.23 for allele A). Allele A of SNP rs3807989 was also associated with a decreased level of LDL cholesterol. Although rs3807989 is a tagSNP for both CAV1 and nearby CAV2, allele A of SNP rs3807989 was associated with an increased expression level of CAV1 (both mRNA and protein), but not CAV2. CONCLUSIONS: The data in this study demonstrated that rs3807989 at the CAV1/CAV2 locus was associated with significant risk of CAD and MI by increasing expression of CAV1 (but not CAV2). Thus, CAV1 becomes a strong candidate susceptibility gene for CAD/MI in humans.

11 Article Candidate pathway-based genome-wide association studies identify novel associations of genomic variants in the complement system associated with coronary artery disease. 2014

Xu, Chengqi / Yang, Qin / Xiong, Hongbo / Wang, Longfei / Cai, Jianping / Wang, Fan / Li, Sisi / Chen, Jing / Wang, Chuchu / Wang, Dan / Xiong, Xin / Wang, Pengyun / Zhao, Yuanyuan / Wang, Xiaojing / Huang, Yufeng / Chen, Shanshan / Yin, Dan / Li, Xiuchun / Liu, Ying / Liu, Jinqiu / Wang, Jingjing / Li, Hui / Ke, Tie / Ren, Xiang / Wu, Yanxia / Wu, Gang / Wan, Jing / Zhang, Rongfeng / Wu, Tangchun / Wang, Junhan / Xia, Yunlong / Yang, Yanzong / Cheng, Xiang / Liao, Yuhua / Chen, Qiuyun / Zhou, Yanhong / He, Qing / Tu, Xin / Wang, Qing K. · ·Circ Cardiovasc Genet · Pubmed #25249547.

ABSTRACT: BACKGROUND: Genomic variants identified by genome-wide association studies (GWAS) explain <20% of heritability of coronary artery disease (CAD), thus many risk variants remain missing for CAD. Identification of new variants may unravel new biological pathways and genetic mechanisms for CAD. To identify new variants associated with CAD, we developed a candidate pathway-based GWAS by integrating expression quantitative loci analysis and mining of GWAS data with variants in a candidate pathway. METHODS AND RESULTS: Mining of GWAS data was performed to analyze variants in 32 complement system genes for positive association with CAD. Functional variants in genes showing positive association were then identified by searching existing expression quantitative loci databases and validated by real-time reverse transcription polymerase chain reaction. A follow-up case-control design was then used to determine whether the functional variants are associated with CAD in 2 independent GeneID Chinese populations. Candidate pathway-based GWAS identified positive association between variants in C3AR1 and C6 and CAD. Two functional variants, rs7842 in C3AR1 and rs4400166 in C6, were found to be associated with expression levels of C3AR1 and C6, respectively. Significant association was identified between rs7842 and CAD (P=3.99×10(-6); odds ratio, 1.47) and between rs4400166 and CAD (P=9.30×10(-3); odds ratio, 1.24) in the validation cohort. The significant findings were confirmed in the replication cohort (P=1.53×10(-5); odds ratio, 1.37 for rs7842; P=8.41×10(-3); odds ratio, 1.21 for rs4400166). CONCLUSIONS: Integration of GWAS with biological pathways and expression quantitative loci is effective in identifying new risk variants for CAD. Functional variants increasing C3AR1 and C6 expression were shown to confer significant risk of CAD for the first time.

12 Article Regulation of CARD8 expression by ANRIL and association of CARD8 single nucleotide polymorphism rs2043211 (p.C10X) with ischemic stroke. 2014

Bai, Ying / Nie, Shaofang / Jiang, Guiqing / Zhou, Yingchao / Zhou, Mengchen / Zhao, Yuanyuan / Li, Sisi / Wang, Fan / Lv, Qiulun / Huang, Yufeng / Yang, Qin / Li, Qingxian / Li, Yue / Xia, Yunlong / Liu, Ying / Liu, Jinqiu / Qian, Jin / Li, Bin / Wu, Gang / Wu, Yanxia / Wang, Binbin / Cheng, Xiang / Yang, Yanzong / Ke, Tie / Li, Hui / Ren, Xiang / Ma, Xu / Liao, Yuhua / Xu, Chengqi / Tu, Xin / Wang, Qing K. ·From the Key Laboratory of Molecular Biophysics of the Ministry of Education, Cardio-X Institute (Y.B., G.J., Yingchao Zhou, M.Z., Yuanyuan Zhao, S.L., F.W., Q. Lu, Y.H., Q.Y., T.K., H.L., X.R., C.X., X.T., Q.K.W.), and College of Life Science and Technology and Center for Human Genome Research, Institute of Cardiology (S.N., X.C., Y. Liao), Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China · Department of Cardiology, Jining Medical College Affiliated Hospital, Jining, China (Q. Li) · Department of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China (Y. Li) · Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, China (Y.X., Y. Liu, J.L., Y.Y.) · Department of Cardiology, Suizhou Central Hospital, Suizhou, China (J.Q.) · Department of Cardiology, Xiangyang Central Hospital, Xiangyang, China (B.L.) · Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (G.W.) · Department of Cardiology, Wuhan No. 1 Hospital, Wuhan, China (Y.W.) · Research Institute of the National Population and Family Planning Commission, Beijing, China (B.W., X.M.) · and Department of Molecular Cardiology, Center for Cardiovascular Genetics, Lerner Research Institute, Cleveland Clinic, OH (Q.K.W.). ·Stroke · Pubmed #24385277.

ABSTRACT: BACKGROUND AND PURPOSE: ANRIL has long been considered as the strongest candidate gene at the 9p21 locus, robustly associated with stroke and coronary artery disease. However, the underlying molecular mechanism remains unknown. The present study works to elucidate such a mechanism. METHODS: Using expression quantitative loci analysis, we identified potential genes whose expression may be influenced by genetic variation in ANRIL. To verify the identified gene(s), knockdown and overexpression of ANRIL were evaluated in human umbilical vein endothelial cells and HepG2 cells. Ischemic stroke and coronary artery disease risk were then evaluated in the gene(s) demonstrated to be mediated by ANRIL in 3 populations of Chinese Han ancestry: 2 ischemic stroke populations consisting of the Central China cohort (903 cases and 873 controls) and the Northern China cohort (816 cases and 879 controls) and 1 coronary artery disease cohort consisting of 772 patients and 873 controls. RESULTS: Expression quantitative loci analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and overexpression of ANRIL increasing CARD8 expression. The minor T allele of a previously identified CARD8 variant (rs2043211) was found to be significantly associated with a protective effect of ischemic stroke under the recessive model in 2 independent stroke cohorts. No significant association was found between rs2043211 and coronary artery disease. CONCLUSIONS: CARD8 is a downstream target gene regulated by ANRIL. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.

13 Article Meta-analysis identifies robust association between SNP rs17465637 in MIA3 on chromosome 1q41 and coronary artery disease. 2013

Li, Xiuchun / Huang, Yufeng / Yin, Dan / Wang, Dan / Xu, Chengqi / Wang, Fan / Yang, Qin / Wang, Xiaojing / Li, Sisi / Chen, Shanshan / Xiong, Xin / Huang, Yuan / Zhao, Yuanyuan / Wang, Li / Zhu, Xuan / Su, Zhenhong / Zhou, Bisheng / Zhang, Yuting / Wang, Longfei / Chang, Le / Xu, Chaoping / Li, Hui / Ke, Tie / Ren, Xiang / Cheng, Xiang / Yang, Yanzong / Liao, Yuhua / Tu, Xin / Wang, Qing K. ·Key Laboratory of Molecular Biophysics of the Ministry of Education, Cardio-X Institute, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, China. ·Atherosclerosis · Pubmed #24125424.

ABSTRACT: Several large-scale meta-GWAS identified significant association between SNP rs17465637 in the MIA3 gene and coronary artery disease (CAD) in the European ancestry populations. However, three follow-up replication studies in the Chinese populations yielded inconsistent results. In order to unequivocally determine whether SNP rs17465637 is associated with CAD, we performed an independent case control association study in the Chinese Han population and a follow-up large scale meta-analysis for SNP rs17465637. Our study included 2503 CAD patients and 2920 non-CAD controls of the Chinese Han origin. A significant association was found between SNP rs17465637 and CAD (P = 0.01, OR = 1.11). Meta-analysis included 7263 CAD patients and 8347 controls combined from five Asian populations. The association between SNP rs17465637 and CAD became highly significant (P = 4.97 × 10(-5), OR = 1.11). Similar analysis also identified significant association between SNP rs17465637 and MI (2424 cases vs. 6,536controls; P = 5.00 × 10(-3), OR = 1.10). We conclude that SNP rs17465637 in MIA3 is indeed a genetic risk factor for CAD across different ethnic populations.

14 Article The IL-33-ST2L pathway is associated with coronary artery disease in a Chinese Han population. 2013

Tu, Xin / Nie, Shaofang / Liao, Yuhua / Zhang, Hongsong / Fan, Qian / Xu, Chengqi / Bai, Ying / Wang, Fan / Ren, Xiang / Tang, Tingting / Xia, Ni / Li, Sisi / Huang, Yuan / Liu, Juan / Yang, Qing / Zhao, Yuanyuan / Lv, Qiulun / Li, Qingxian / Li, Yue / Xia, Yunlong / Qian, Jin / Li, Bin / Wu, Gang / Wu, Yanxia / Yang, Yan / Wang, Qing K / Cheng, Xiang. ·Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan 430074, China. ·Am J Hum Genet · Pubmed #24075188.

ABSTRACT: The effects of interleukin-33 (IL-33) on the immune system have been clearly demonstrated; however, in cardiovascular diseases, especially in coronary artery disease (CAD), these effects have not yet been clarified. In this study, we investigate the genetic role of the IL-33-ST2L pathway in CAD. We performed three-stage case-control association analyses on a total of 4,521 individuals with CAD and 4,809 controls via tag SNPs in the genes encoding IL-33 and ST2L-IL-1RL1. One tag SNP in each gene was significantly associated with CAD (rs7025417(T) in IL33, padj = 1.19 × 10(-28), OR = 1.39, 95% CI: 1.31-1.47; rs11685424(G) in IL1RL1, padj = 6.93 × 10(-30), OR = 1.40, 95% CI: 1.32-1.48). Combining significant variants in two genes, the risk for CAD increased nearly 5-fold (padj = 8.90 × 10(-21), OR = 4.98, 95% CI: 3.56-6.97). Traditional risk factors for CAD were adjusted for the association studies by SPSS with logistic regression analysis. With the two variants above, both located within the gene promoter regions, reporter gene analysis indicated that the rs7025417 C>T and rs11685424 A>G changes resulted in altered regulation of IL33 and IL1RL1 gene expression, respectively (p < 0.005). Further studies revealed that the rs7025417 genotype was significantly associated with plasma IL-33 levels in the detectable subjects (n = 227, R(2) = 0.276, p = 1.77 × 10(-17)): the level of IL-33 protein increased with the number of rs7025417 risk (T) alleles. Based on genetic evidence in humans, the IL-33-ST2L pathway appears to have a causal role in the development of CAD, highlighting this pathway as a valuable target for the prevention and treatment of CAD.

15 Article Association factors of target organ damage: analysis of 17,682 elderly hypertensive patients in China. 2011

Cui, Hua / Wang, Fan / Fan, Li / Hu, Yi-Xin / Hu, Guo-Liang / Liu, Lin / Hong, Chang-Ming. ·Nanlou Cardiology Department 2, Beijing 100853, China. ·Chin Med J (Engl) · Pubmed #22340223.

ABSTRACT: BACKGROUND: Hypertensive target organ damage (TOD) is the main reason for mortality or disability in elderly hypertensive patients. The studies on TOD of hypertension in Asia, especially in Chinese elderly hypertensive patients, are very limited. The aim of this study was to evaluate the prevalence and correlative factors of TOD in older Chinese hypertensive inpatients. METHODS: This is a retrospective survey and data were collected from the computerized medical files of hypertensive inpatients from January of 1993 to December of 2008. The analysis was done on 17 682 inpatients, aged 60 years or older, with a diagnosis of essential hypertension (EH). The evidence of hypertensive TOD and associated factors with TOD were collected. RESULTS: The prevalence of any hypertensive target organ involvement among these subjects was high. In multivariable Logistic regressions adjusted for potentially confounding factors, older age, male gender, diabetes, EH grade 3, systolic blood pressure (SBP), and low-density lipoprotein cholesterol (LDL-C), were independently associated with coronary artery disease. Age, duration of EH, EH grade 3, SBP, pulse pressure (PP), and homocysteine (Hcy) were independently associated with cerebrovascular disease. Age, diabetes, duration of EH, EH grade 3, SBP, PP and estimated glomerular filtration rate (eGFR) were independently associated with chronic kidney disease. Male gender, EH grade 3 and SBP were independently associated with aortic dissection. CONCLUSIONS: The prevalence of hypertensive TOD is high in older Chinese hypertensive inpatients. Various cardiovascular risk factors are associated with hypertensive TOD. The level of SBP and severe hypertension (grade 3 hypertension) are common independent risk factors of TOD.

16 Article Genome-wide association identifies a susceptibility locus for coronary artery disease in the Chinese Han population. 2011

Wang, Fan / Xu, Cheng-Qi / He, Qing / Cai, Jian-Ping / Li, Xiu-Chun / Wang, Dan / Xiong, Xin / Liao, Yu-Hua / Zeng, Qiu-Tang / Yang, Yan-Zong / Cheng, Xiang / Li, Cong / Yang, Rong / Wang, Chu-Chu / Wu, Gang / Lu, Qiu-Lun / Bai, Ying / Huang, Yu-Feng / Yin, Dan / Yang, Qing / Wang, Xiao-Jing / Dai, Da-Peng / Zhang, Rong-Feng / Wan, Jing / Ren, Jiang-Hua / Li, Si-Si / Zhao, Yuan-Yuan / Fu, Fen-Fen / Huang, Yuan / Li, Qing-Xian / Shi, Sheng-Wei / Lin, Nan / Pan, Zhen-Wei / Li, Yue / Yu, Bo / Wu, Yan-Xia / Ke, Yu-He / Lei, Jian / Wang, Nan / Luo, Chun-Yan / Ji, Li-Ying / Gao, Lian-Jun / Li, Lei / Liu, Hui / Huang, Er-Wen / Cui, Jin / Jia, Na / Ren, Xiang / Li, Hui / Ke, Tie / Zhang, Xian-Qin / Liu, Jing-Yu / Liu, Mu-Gen / Xia, Hao / Yang, Bo / Shi, Li-Song / Xia, Yun-Long / Tu, Xin / Wang, Qing K. ·Key Laboratory of Molecular Biophysics of the Ministry of Education, Cardio-X Institute, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, China. ·Nat Genet · Pubmed #21378986.

ABSTRACT: Coronary artery disease (CAD) causes more than 700,000 deaths each year in China. Previous genome-wide association studies (GWAS) in populations of European ancestry identified several genetic loci for CAD, but no such study has yet been reported in the Chinese population. Here we report a three-stage GWAS in the Chinese Han population. We identified a new association between rs6903956 in a putative gene denoted as C6orf105 on chromosome 6p24.1 and CAD (P = 5.00 × 10⁻³, stage 2 validation; P = 3.00 × 10⁻³, P = 1.19 × 10⁻⁸ and P = 4.00 × 10⁻³ in three independent stage 3 replication populations; P = 4.87 × 10⁻¹², odds ratio = 1.51 in the combined population). The minor risk allele A of rs6903956 is associated with decreased C6orf105 mRNA expression. We report the first GWAS for CAD in the Chinese Han population and identify a SNP, rs6903956, in C6orf105 associated with susceptibility to CAD in this population.

17 Article The same chromosome 9p21.3 locus is associated with type 2 diabetes and coronary artery disease in a Chinese Han population. 2011

Cheng, Xiang / Shi, Lisong / Nie, Shaofang / Wang, Fan / Li, Xiuchun / Xu, Chengqi / Wang, Pengyun / Yang, Baofeng / Li, Qingxian / Pan, Zhenwei / Li, Yue / Xia, Hao / Zheng, Chenhong / Ke, Yuhe / Wu, Yanxia / Tang, Tingting / Yan, Xinxin / Yang, Yan / Xia, Ni / Yao, Rui / Wang, Binbin / Ma, Xu / Zeng, Qiutang / Tu, Xin / Liao, Yuhua / Wang, Qing K. ·Institute of Cardiology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. ·Diabetes · Pubmed #21270277.

ABSTRACT: OBJECTIVE: Recent genome-wide association studies (GWAS) revealed that a 9p21.3 locus was associated with type 2 diabetes. In this study, we carried out a large-scale case-control study in the GeneID Chinese Han population to 1) further replicate the association of 9p21.3 type 2 diabetes GWAS single nucleotide polymorphisms (SNPs) and 2) assess the association of these SNPs with coronary artery disease. RESEARCH DESIGN AND METHODS: Three SNPs (rs2383208, rs10811661, and rs10757283) were genotyped in two GeneID cohorts of 3,167 Chinese Han individuals. Case-control association design was used to determine the association of the SNPs with type 2 diabetes and coronary artery disease. Gensini scores were calculated in the coronary artery disease subjects and were tested for association with the variants. Multivariate logistic regressions were performed on association studies. RESULTS: The association between two of the three SNPs and type 2 diabetes was replicated in the GeneID population (rs2383208, P = 0.936; rs10811661-T, P = 0.02, odds ratio [OR] = 1.23; rs10757283-C, P = 0.003, OR = 1.30). The same two SNPs also contributed to the risk of coronary artery disease (CAD) (rs10811661-T, P = 0.002, OR = 1.19; rs10757283-C, P = 0.003, OR = 1.18). In addition, rs10757283 was associated with severity of coronary atherosclerosis estimated by the Gensini scoring system (risk allele C, quantitative-trait regression adjusted P = 0.002). CONCLUSIONS: For the first time to our knowledge, our results indicated that the same 9p21.3 locus, represented by SNPs rs10811661 and rs10757283, contributed to the risk of type 2 diabetes and coronary artery disease in our GeneID Chinese Han population.

18 Article Significant association of SNP rs2106261 in the ZFHX3 gene with atrial fibrillation in a Chinese Han GeneID population. 2011

Li, Cong / Wang, Fan / Yang, Yanzong / Fu, Fenfen / Xu, Chengqi / Shi, Lisong / Li, Sisi / Xia, Yunlong / Wu, Gang / Cheng, Xiang / Liu, Hui / Wang, Chuchu / Wang, Pengyun / Hao, Jianjun / Ke, Yuhe / Zhao, Yuanyuan / Liu, Mugen / Zhang, Rongfeng / Gao, Lianjun / Yu, Bo / Zeng, Qiutang / Liao, Yuhua / Yang, Bo / Tu, Xin / Wang, Qing K. ·Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, China. ·Hum Genet · Pubmed #21107608.

ABSTRACT: Atrial fibrillation (AF) is the most common cardiac rhythm disorder at the clinical setting and accounts for up to 15% of all strokes. Recent genome-wide association studies (GWAS) identified two single nucleotide polymorphisms (SNPs), rs2106261 and rs7193343 in ZFHX3 (zinc finger homeobox 3 gene) and rs13376333 in KCNN3 (encoding a potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3) that showed significant association with AF in multiple populations of European ancestry. Here, we studied a Chinese Han, GeneID cohort consisting of 650 AF patients and 1,447 non-AF controls to test whether the GWAS findings on ZFHX3/KCNN3 and AF can be expanded to a different ethnic population. No significant association was detected for rs7193343 in ZFHX3 and rs13376333 in KCNN3. However, significant association was identified between rs2106261 in ZFHX3 and AF in the GeneID population for both allelic frequencies (P=0.001 after adjusting for covariates of age, gender, hypertension, coronary artery disease, and diabetes mellitus; OR=1.32), and genotypic frequencies assuming either an additive or recessive model (OR=1.29, P=0.001 and OR=1.77, P =0.00018, respectively). When only lone AF cases were analyzed, the association remained significant (OR=1.50, P=0.001 for allelic association; OR=1.45, P=0.001 for an additive model; OR=2.24, P=0.000043 for a recessive model). Our results indicate that rs2106261 in ZFHX3 confers a significant risk of AF in a Chinese Han population. The study expands the association between ZFHX3 and AF to a non-European ancestry population and provides the first evidence of a cross-race susceptibility of the 16q22 AF locus.

19 Article Minor allele C of chromosome 1p32 single nucleotide polymorphism rs11206510 confers risk of ischemic stroke in the Chinese Han population. 2010

Xu, Chengqi / Wang, Fan / Wang, Binbin / Li, Xiuchun / Li, Cong / Wang, Dan / Xiong, Xin / Wang, Pengyun / Lu, Qiulun / Wang, Xiaojing / Yang, Qin / Yin, Dan / Huang, Yufeng / Ji, Liying / Wang, Nan / Chen, Shanshan / Cheng, Xiang / Liao, Yuhua / Ma, Xu / Su, Dingfeng / Chen, Guohua / Xia, Hao / Shi, Lisong / Tu, Xin / Wang, Qing K. ·Key Laboratory of Molecular Biophysics of Ministry of Education, Integrated Traditional Chinese and Western Medicine Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Peoples Republic of China. ·Stroke · Pubmed #20576952.

ABSTRACT: BACKGROUND AND PURPOSE: Genome-wide association studies found that the common allele T of single nucleotide polymorphism rs11206510 on chromosome 1p32 was associated with increased low-density lipoprotein-cholesterol levels (LDL-C) and with risk of coronary artery disease (CAD) in white populations. The goals of this study are to determine whether rs11206510 is associated with LDL-C and CAD in a different ethnic population, namely a Chinese cohort, and to investigate whether rs11206510 is associated with ischemic stroke. METHODS: The association of rs11206510 with LDL-C was analyzed in 1415 Chinese Han subjects. The CAD study utilized a GeneID cohort with 1543 CAD patients and 1240 controls. For stroke studies, 2 independent cohorts were used and included the GeneID North cohort, with 1205 cases and 1205 controls, and the GeneID Central cohort, with 692 cases and 882 controls. RESULTS: Different from white populations, the minor allele C of rs11206510 was associated with increased LDL-C levels in the Chinese Han population (adjusted P=0.002) and conferred risk of early-onset CAD (380 cases vs 1240 controls; adjusted P=0.002, odds ratio, 1.89), but not with overall CAD (adjusted P=0.82). The allelic association with ischemic stroke was highly significant in 2 independent cohorts, with adjusted P=1.13x10(-5) (odds ratio,1.71) in the GeneID North cohort and adjusted P=9.32x10(-5) (odds ratio, 1.70) in the GeneID Central cohort. Genotypic association was also significant for both early-onset CAD and ischemic stroke. CONCLUSIONS: Our results indicate that single nucleotide polymorphism rs11206510 is associated with LDL-C levels and early-onset CAD in the Chinese Han population. For the first time to our knowledge, this study also demonstrates that rs11206510 confers a significant risk of ischemic stroke.