SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Lieb Wolfgang) "

Sökning: WFRF:(Lieb Wolfgang)

  • Resultat 21-26 av 26
  • Föregående 12[3]
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
21.
  • Kato, Norihiro, et al. (författare)
  • Trans-ancestry genome-wide association study identifies 12 genetic loci influencing blood pressure and implicates a role for DNA methylation.
  • 2015
  • Ingår i: Nature Genetics. - : Nature Publishing Group. - 1546-1718 .- 1061-4036. ; 47:11, s. 93-1282
  • Tidskriftsartikel (refereegranskat)abstract
    • We carried out a trans-ancestry genome-wide association and replication study of blood pressure phenotypes among up to 320,251 individuals of East Asian, European and South Asian ancestry. We find genetic variants at 12 new loci to be associated with blood pressure (P = 3.9 × 10(-11) to 5.0 × 10(-21)). The sentinel blood pressure SNPs are enriched for association with DNA methylation at multiple nearby CpG sites, suggesting that, at some of the loci identified, DNA methylation may lie on the regulatory pathway linking sequence variation to blood pressure. The sentinel SNPs at the 12 new loci point to genes involved in vascular smooth muscle (IGFBP3, KCNK3, PDE3A and PRDM6) and renal (ARHGAP24, OSR1, SLC22A7 and TBX2) function. The new and known genetic variants predict increased left ventricular mass, circulating levels of NT-proBNP, and cardiovascular and all-cause mortality (P = 0.04 to 8.6 × 10(-6)). Our results provide new evidence for the role of DNA methylation in blood pressure regulation.
  •  
22.
  • Nikpay, Majid, et al. (författare)
  • A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease
  • 2015
  • Ingår i: Nature Genetics. - : Nature Publishing Group. - 1546-1718 .- 1061-4036. ; 47:10, s. 1121-1121
  • Tidskriftsartikel (refereegranskat)abstract
    • Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association study (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of similar to 185,000 CAD cases and controls, interrogating 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants. In addition to confirming most known CAD-associated loci, we identified ten new loci (eight additive and two recessive) that contain candidate causal genes newly implicating biological processes in vessel walls. We observed intralocus allelic heterogeneity but little evidence of low-frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD, showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect size.
  •  
23.
  • Stitziel, Nathan O., et al. (författare)
  • Coding variation in ANGPTL4, LPL, and SVEP1 and the risk of coronary disease
  • Ingår i: New England Journal of Medicine. - : Massachusetts Medical Society. - 0028-4793 .- 1533-4406. ; 374:12, s. 1134-1144
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The discovery of low-frequency coding variants affecting the risk of coronary artery disease has facilitated the identification of therapeutic targets. METHODS: Through DNA genotyping, we tested 54,003 coding-sequence variants covering 13,715 human genes in up to 72,868 patients with coronary artery disease and 120,770 controls who did not have coronary artery disease. Through DNA sequencing, we studied the effects of loss-of-function mutations in selected genes. RESULTS: We confirmed previously observed significant associations between coronary artery disease and low-frequency missense variants in the genes LPA and PCSK9. We also found significant associations between coronary artery disease and low-frequency missense variants in the genes SVEP1 (p.D2702G; minor-allele frequency, 3.60%; odds ratio for disease, 1.14; P = 4.2×10-10) and ANGPTL4 (p.E40K; minorallele frequency, 2.01%; odds ratio, 0.86; P = 4.0×10-8), which encodes angiopoietin-like 4. Through sequencing of ANGPTL4, we identified 9 carriers of loss-of-function mutations among 6924 patients with myocardial infarction, as compared with 19 carriers among 6834 controls (odds ratio, 0.47; P = 0.04); carriers of ANGPTL4 loss-of-function alleles had triglyceride levels that were 35% lower than the levels among persons who did not carry a loss-of-function allele (P = 0.003). ANGPTL4 inhibits lipoprotein lipase; we therefore searched for mutations in LPL and identified a loss-of-function variant that was associated with an increased risk of coronary artery disease (p.D36N; minor-allele frequency, 1.9%; odds ratio, 1.13; P = 2.0×10-4) and a gain-of-function variant that was associated with protection from coronary artery disease (p.S447∗; minor-allele frequency, 9.9%; odds ratio, 0.94; P = 2.5×10-7). CONCLUSIONS: We found that carriers of loss-of-function mutations in ANGPTL4 had triglyceride levels that were lower than those among noncarriers; these mutations were also associated with protection from coronary artery disease. (Funded by the National Institutes of Health and others).
  •  
24.
  • Surendran, Praveen, et al. (författare)
  • Trans-ancestry meta-analyses identify rare and common variants associated with blood pressure and hypertension
  • Ingår i: Nature Genetics. - : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 48:10, s. 1151-1161
  • Tidskriftsartikel (refereegranskat)abstract
    • High blood pressure is a major risk factor for cardiovascular disease and premature death. However, there is limited knowledge on specific causal genes and pathways. To better understand the genetics of blood pressure, we genotyped 242,296 rare, low-frequency and common genetic variants in up to 192,763 individuals and used -1/4155,063 samples for independent replication. We identified 30 new blood pressure- or hypertension-associated genetic regions in the general population, including 3 rare missense variants in RBM47, COL21A1 and RRAS with larger effects (>1.5 mm Hg/allele) than common variants. Multiple rare nonsense and missense variant associations were found in A2ML1, and a low-frequency nonsense variant in ENPEP was identified. Our data extend the spectrum of allelic variation underlying blood pressure traits and hypertension, provide new insights into the pathophysiology of hypertension and indicate new targets for clinical intervention.
  •  
25.
  • van Rheenen, Wouter, et al. (författare)
  • Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis
  • 2016
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 48:9, s. 1043-1048
  • Tidskriftsartikel (refereegranskat)abstract
    • To elucidate the genetic architecture of amyotrophic lateral sclerosis (ALS) and find associated loci, we assembled a custom imputation reference panel from whole-genome-sequenced patients with ALS and matched controls (n = 1,861). Through imputation and mixed-model association analysis in 12,577 cases and 23,475 controls, combined with 2,579 cases and 2,767 controls in an independent replication cohort, we fine-mapped a new risk locus on chromosome 21 and identified C21orf2 as a gene associated with ALS risk. In addition, we identified MOBP and SCFD1 as new associated risk loci. We established evidence of ALS being a complex genetic trait with a polygenic architecture. Furthermore, we estimated the SNP-based heritability at 8.5%, with a distinct and important role for low-frequency variants (frequency 1-10%). This study motivates the interrogation of larger samples with full genome coverage to identify rare causal variants that underpin ALS risk.
  •  
26.
  • Wild, Philipp S., et al. (författare)
  • Large-scale genome-wide analysis identifies genetic variants associated with cardiac structure and function
  • Ingår i: Journal of Clinical Investigation. - : Am Soc Clin Investig. - 0021-9738 .- 1558-8238. ; 127:5, s. 1798-1812
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND. Understanding the genetic architecture of cardiac structure and function may help to prevent and treat heart disease. This investigation sought to identify common genetic variations associated with inter-individual variability in cardiac structure and function. METHODS. A GWAS meta-analysis of echocardiographic traits was performed, including 46,533 individuals from 30 studies (EchoGen consortium). The analysis included 16 traits of left ventricular (LV) structure, and systolic and diastolic function. RESULTS. The discovery analysis included 21 cohorts for structural and systolic function traits (n = 32,212) and 17 cohorts for diastolic function traits (n = 21,852). Replication was performed in 5 cohorts (n = 14,321) and 6 cohorts (n = 16,308), respectively. Besides 5 previously reported loci, the combined meta-analysis identified 10 additional genome-wide significant SNPs: rs12541595 near MTSS1 and rs10774625 in ATXN2 for LV end-diastolic internal dimension; rs806322 near KCNRG, rs4765663 in CACNA1C, rs6702619 near PALMD, rs7127129 in TMEM16A, rs11207426 near FGGY, rs17608766 in GOSR2, and rs17696696 in CFDP1 for aortic root diameter; and rs12440869 in IQCH for Doppler transmitral A-wave peak velocity. Findings were in part validated in other cohorts and in GWAS of related disease traits. The genetic loci showed associations with putative signaling pathways, and with gene expression in whole blood, monocytes, and myocardial tissue. CONCLUSION. The additional genetic loci identified in this large meta-analysis of cardiac structure and function provide insights into the underlying genetic architecture of cardiac structure and warrant follow-up in future functional studies.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 21-26 av 26
  • Föregående 12[3]
Typ av publikation
tidskriftsartikel (26)
Typ av innehåll
refereegranskat (26)
Författare/redaktör
Lieb, Wolfgang (26)
Franke, Andre (14)
Lieb, W (12)
Esko, Tonu (12)
Uitterlinden, Andre ... (11)
Meitinger, Thomas (11)
visa fler...
Meisinger, Christa (11)
Melander, Olle (10)
Gieger, Christian (9)
Peters, Annette (9)
Samani, Nilesh J. (9)
Loos, Ruth J F (9)
Franke, A (8)
Jukema, J. Wouter (8)
Deloukas, Panos (8)
Wichmann, H. Erich (8)
Metspalu, Andres (8)
Kathiresan, Sekar (8)
Kleber, Marcus E. (8)
Hengstenberg, Christ ... (8)
Schunkert, Heribert (8)
Lind, Lars (7)
Hofman, Albert (7)
Waldenberger, Melani ... (7)
van der Harst, Pim (7)
Müller-Nurasyid, Mar ... (7)
Franco, Oscar H (7)
Boerwinkle, Eric (7)
Hall, Alistair S. (7)
Erdmann, Jeanette (7)
Heid, Iris M (7)
Raitakari, Olli T (6)
Brenner, Hermann (6)
Teumer, Alexander (6)
Gudnason, Vilmundur (6)
Psaty, Bruce M. (6)
Salomaa, Veikko (6)
Strauch, Konstantin (6)
Palmer, Colin N. A. (6)
Harris, Tamara B (6)
Kronenberg, Florian (6)
Asselbergs, Folkert ... (6)
Rivadeneira, Fernand ... (6)
Morris, Andrew P (6)
Hwang, Shih-Jen (6)
Verweij, Niek (6)
Felix, Janine F. (6)
Lindgren, Cecilia M. (6)
Dehghan, Abbas (6)
Lu, Yingchang (6)
visa färre...
Lärosäte
Lunds universitet (13)
Umeå universitet (8)
Uppsala universitet (8)
Karolinska Institutet (6)
Göteborgs universitet (5)
Linköpings universitet (2)
visa fler...
Högskolan Dalarna (2)
Stockholms universitet (1)
Örebro universitet (1)
visa färre...
Språk
Engelska (26)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (25)
Naturvetenskap (1)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy