Publications
403 results found
Desikan RS, Schork AJ, Wang Y, et al., 2015, Polygenic Overlap Between C-Reactive Protein, Plasma Lipids, and Alzheimer Disease, CIRCULATION, Vol: 131, Pages: 2061-2069, ISSN: 0009-7322
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- Citations: 99
Muka T, Kiefte-de Jong JC, Hofman A, et al., 2015, Polyunsaturated Fatty Acids and Serum C-Reactive Protein The Rotterdam Study, AMERICAN JOURNAL OF EPIDEMIOLOGY, Vol: 181, Pages: 846-856, ISSN: 0002-9262
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- Citations: 36
Ghanbari M, Franco OH, de Looper HWJ, et al., 2015, Genetic Variations in MicroRNA-Binding Sites Affect MicroRNA-Mediated Regulation of Several Genes Associated With Cardio-metabolic Phenotypes, CIRCULATION-CARDIOVASCULAR GENETICS, Vol: 8, Pages: 473-486, ISSN: 1942-325X
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- Citations: 54
Chaker L, Baumgartner C, den Elzen WPJ, et al., 2015, Subclinical Hypothyroidism and the Risk of Stroke Events and Fatal Stroke: An Individual Participant Data Analysis, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 100, Pages: 2181-2191, ISSN: 0021-972X
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- Citations: 121
Steenaard RV, Ligthart S, Stolk L, et al., 2015, Tobacco smoking is associated with methylation of genes related to coronary artery disease, CLINICAL EPIGENETICS, Vol: 7, ISSN: 1868-7075
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- Citations: 51
Fall T, Hagg S, Ploner A, et al., 2015, Age- and Sex-Specific Causal Effects of Adiposity on Cardiovascular Risk Factors, DIABETES, Vol: 64, Pages: 1841-1852, ISSN: 0012-1797
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- Citations: 52
Gorski M, Tin A, Garnaas M, et al., 2015, Genome-wide association study of kidney function decline in individuals of European descent, KIDNEY INTERNATIONAL, Vol: 87, Pages: 1017-1029, ISSN: 0085-2538
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- Citations: 99
Chaker L, Buitendijk GHS, Dehghan A, et al., 2015, Thyroid function and age-related macular degeneration: a prospective population-based cohort study - <i>the Rotterdam Study</i>, BMC MEDICINE, Vol: 13, ISSN: 1741-7015
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- Citations: 45
Freitag DF, Butterworth AS, Willeit P, et al., 2015, Cardiometabolic effects of genetic upregulation of the interleukin 1 receptor antagonist: a Mendelian randomisation analysis, LANCET DIABETES & ENDOCRINOLOGY, Vol: 3, Pages: 243-253, ISSN: 2213-8587
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- Citations: 90
Yu B, Li AH, Muzny D, et al., 2015, Association of Rare Loss-Of-Function Alleles in <i>HAL</i>, Serum Histidine Levels and Incident Coronary Heart Disease, CIRCULATION-CARDIOVASCULAR GENETICS, Vol: 8, Pages: 351-355, ISSN: 1942-325X
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- Citations: 33
Postmus I, Deelen J, Sedaghat S, et al., 2015, LDL cholesterol still a problem in old age? A Mendelian randomization study, INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 44, Pages: 604-612, ISSN: 0300-5771
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- Citations: 38
Haegg S, Fall T, Ploner A, et al., 2015, Adiposity as a cause of cardiovascular disease: a Mendelian randomization study, INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 44, Pages: 578-586, ISSN: 0300-5771
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- Citations: 98
de Vries PS, Kavousi M, Ligthart S, et al., 2015, Incremental predictive value of 152 single nucleotide polymorphisms in the 10-year risk prediction of incident coronary heart disease: the Rotterdam Study, INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 44, Pages: 682-688, ISSN: 0300-5771
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- Citations: 41
Huffman JE, Albrecht E, Teumer A, et al., 2015, Modulation of Genetic Associations with Serum Urate Levels by Body-Mass-Index in Humans, PLOS ONE, Vol: 10, ISSN: 1932-6203
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- Citations: 32
Huan T, Esko T, Peters MJ, et al., 2015, A meta-analysis of gene expression signatures of blood pressure and hypertension, PLoS Genetics, Vol: 11, ISSN: 1553-7390
Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%–9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension.
Ligthart S, de Vries PS, Uitterlinden AG, et al., 2015, Pleiotropy among common genetic loci identified for cardiometabolic disorders and C-reactive protein, PLoS One, Vol: 10, Pages: 1-17, ISSN: 1932-6203
Pleiotropic genetic variants have independent effects on different phenotypes. C-reactive protein (CRP) is associated with several cardiometabolic phenotypes. Shared genetic backgrounds may partially underlie these associations. We conducted a genome-wide analysis to identify the shared genetic background of inflammation and cardiometabolic phenotypes using published genome-wide association studies (GWAS). We also evaluated whether the pleiotropic effects of such loci were biological or mediated in nature. First, we examined whether 283 common variants identified for 10 cardiometabolic phenotypes in GWAS are associated with CRP level. Second, we tested whether 18 variants identified for serum CRP are associated with 10 cardiometabolic phenotypes. We used a Bonferroni corrected p-value of 1.1×10-04 (0.05/463) as a threshold of significance. We evaluated the independent pleiotropic effect on both phenotypes using individual level data from the Women Genome Health Study. Evaluating the genetic overlap between inflammation and cardiometabolic phenotypes, we found 13 pleiotropic regions. Additional analyses showed that 6 regions (APOC1, HNF1A, IL6R, PPP1R3B, HNF4A and IL1F10) appeared to have a pleiotropic effect on CRP independent of the effects on the cardiometabolic phenotypes. These included loci where individuals carrying the risk allele for CRP encounter higher lipid levels and risk of type 2 diabetes. In addition, 5 regions (GCKR, PABPC4, BCL7B, FTO and TMEM18) had an effect on CRP largely mediated through the cardiometabolic phenotypes. In conclusion, our results show genetic pleiotropy among inflammation and cardiometabolic phenotypes. In addition to reverse causation, our data suggests that pleiotropic genetic variants partially underlie the association between CRP and cardiometabolic phenotypes.
Versmissen J, Oosterveer DM, Yazdanpanah M, et al., 2015, Identifying genetic risk variants for coronary heart disease in familial hypercholesterolemia: an extreme genetics approach, EUROPEAN JOURNAL OF HUMAN GENETICS, Vol: 23, Pages: 381-387, ISSN: 1018-4813
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- Citations: 12
Shungin D, Winkler TW, Croteau-Chonka DC, et al., 2015, New genetic loci link adipose and insulin biology to body fat distribution, NATURE, Vol: 518, Pages: 187-U378, ISSN: 0028-0836
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- Citations: 989
Locke AE, Kahali B, Berndt SI, et al., 2015, Genetic studies of body mass index yield new insights for obesity biology, Nature, Vol: 518, Pages: 197-206, ISSN: 0028-0836
Ghanbari M, Sedaghat S, de Looper HWJ, et al., 2015, The Association of Common Polymorphisms in miR-196a2 with Waist to Hip Ratio and miR-1908 with Serum Lipid and Glucose, OBESITY, Vol: 23, Pages: 495-503, ISSN: 1930-7381
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- Citations: 24
Wessel J, Chu AY, Willems SM, et al., 2015, Low-frequency and rare exome chip variants associate with fasting glucose and type 2 diabetes susceptibility, Nature Communications, Vol: 6, ISSN: 2041-1723
Fasting glucose and insulin are intermediate traits for type 2 diabetes. Here we explore therole of coding variation on these traits by analysis of variants on the HumanExome BeadChipin 60,564 non-diabetic individuals and in 16,491 T2D cases and 81,877 controls. We identify anovel association of a low-frequency nonsynonymous SNV in GLP1R (A316T; rs10305492;MAF ¼ 1.4%) with lower FG (b ¼ 0.09±0.01 mmol l 1, P ¼ 3.4 10 12), T2D risk(OR[95%CI] ¼ 0.86[0.76–0.96], P ¼ 0.010), early insulin secretion (b ¼ 0.07±0.035pmolinsulin mmolglucose 1 , P ¼ 0.048), but higher 2-h glucose (b ¼ 0.16±0.05 mmol l 1,P ¼ 4.3 10 4). We identify a gene-based association with FG at G6PC2(pSKAT ¼ 6.8 10 6) driven by four rare protein-coding SNVs (H177Y, Y207S, R283X andS324P). We identify rs651007 (MAF ¼ 20%) in the first intron of ABO at the putativepromoter of an antisense lncRNA, associating with higher FG (b ¼ 0.02±0.004 mmol l 1,P ¼ 1.3 10 8). Our approach identifies novel coding variant associations and extendsthe allelic spectrum of variation underlying diabetes-related quantitative traits and T2Dsusceptibility.DOI: 10.103
Baumert J, Huang J, McKnight B, et al., 2014, No Evidence for Genome-Wide Interactions on Plasma Fibrinogen by Smoking, Alcohol Consumption and Body Mass Index: Results from Meta-Analyses of 80,607 Subjects, PLOS ONE, Vol: 9, ISSN: 1932-6203
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- Citations: 5
Franceschini N, Hu Y, Reiner AP, et al., 2014, Prospective Associations of Coronary Heart Disease Loci in African Americans Using the MetaboChip: The PAGE Study, PLOS ONE, Vol: 9, ISSN: 1932-6203
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- Citations: 17
Keller MF, Reiner AP, Okada Y, et al., 2014, Trans-ethnic meta-analysis of white blood cell phenotypes, HUMAN MOLECULAR GENETICS, Vol: 23, Pages: 6944-6960, ISSN: 0964-6906
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- Citations: 49
Rodenburg EM, Hofland J, Van Noord C, et al., 2014, Sex-specific differences in the effects of local androgen metabolism in the heart as an indicator for the risk of myocardial infarction, Cardiovascular Endocrinology, Vol: 3, Pages: 134-141
Aim Testosterone influences cardiovascular risk and disease in a sex-specific manner. The more potent androgen 5α-dihydrotestosterone (DHT) can be formed through conversion of testosterone by the enzyme 5α-reductase. We hypothesized that, because of the presence of DHT in coronary and myocardial tissues, a sexually dimorphic effect can be observed if differences exist in genetics or mRNA expression in androgen-metabolizing enzymes. Materials and methods mRNA levels of steroidogenic enzymes and the androgen receptor (AR) were investigated in human myocardial tissue samples. Subsequently, all participants in the baseline cohort of the Rotterdam Study (RSI) with successful genotyping and without prevalent myocardial infarction (MI, N=5199) were recruited to study the association between single nucleotide polymorphisms (SNPs) within SRD5A1, SRD5A2, and AKR1C3 and incident MI using Cox regression models. Significant results were replicated within the Atherosclerosis Risk in Communities cohort and the second cohort of the RSII. Results The expression of SRD5A1, AKR1C3, and AR was found in all myocardial samples, whereas HSD17B3 and SRD5A2 expression levels were low and undetectable, respectively. Myocardial SRD5A1 expression was higher in women than in men. Within SRD5A1, SNP rs248805G>A was significantly associated with incident MI in western European women (hazard ratio 1.49; 95% confidence interval 1.19-1.87). This SNP is tightly linked to the HinfI polymorphism in SRD5A1 (rs248793G>C), of which the minor allele has been associated with a higher DHT/T ratio. Conclusion Genetic variation in SRD5A1 is associated with an increased risk of MI in western European women, possibly because of the sex-specific potential of local androgen conversion and effect.
Ligthart S, Sedaghat S, Ikram MA, et al., 2014, EN-RAGE A Novel Inflammatory Marker for Incident Coronary Heart Disease, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 34, Pages: 2695-2699, ISSN: 1079-5642
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- Citations: 49
Ghanbari M, de Vries PS, de Looper H, et al., 2014, A Genetic Variant in the Seed Region of miR-4513 Shows Pleiotropic Effects on Lipid and Glucose Homeostasis, Blood Pressure, and Coronary Artery Disease, HUMAN MUTATION, Vol: 35, Pages: 1524-1531, ISSN: 1059-7794
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- Citations: 37
Sedaghat S, Pazoki R, Uitterlinden AG, et al., 2014, Association of Uric Acid Genetic Risk Score With Blood Pressure The Rotterdam Study, HYPERTENSION, Vol: 64, Pages: 1061-+, ISSN: 0194-911X
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- Citations: 29
Chaker L, Baumgartner C, Ikram MA, et al., 2014, Subclinical thyroid dysfunction and the risk of stroke: a systematic review and meta-analysis, EUROPEAN JOURNAL OF EPIDEMIOLOGY, Vol: 29, Pages: 791-800, ISSN: 0393-2990
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- Citations: 38
Sedaghat S, Arce FGD, Verwoert GC, et al., 2014, Association of renal function with vascular stiffness in older adults: the Rotterdam study, AGE AND AGEING, Vol: 43, Pages: 827-833, ISSN: 0002-0729
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- Citations: 13
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