rs11810571 - TDRKH

Magnitude 2.2 · 6 studies on file

Reported associations

• Genome-wide analysis identifies novel susceptibility loci for myocardial infarction. - European heart journal (2021) · Hartiala JA, Han Y, Jia Q, Hilser JR, Huang P, Gukasyan J, Schwartzman WS, Cai Z, Biswas S, Trégouët DA, Smith NL, Seldin M, Pan C, Mehrabian M, Lusis AJ, Bazeley P, Sun YV, Liu C, Quyyumi AA, Scholz M, Thiery J, Delgado GE, Kleber ME, März W, Howe LJ, Asselbergs FW, van Vugt M, Vlachojannis GJ, Patel RS, Lyytikäinen LP, Kähönen M, Lehtimäki T, Nieminen TVM, Kuukasjärvi P, Laurikka JO, Chang X, Heng CK, Jiang R, Kraus WE, Hauser ER, Ferguson JF, Reilly MP, Ito K, Koyama S, Kamatani Y, Komuro I, Stolze LK, Romanoski CE, Khan MD, Turner AW, Miller CL, Aherrahrou R, Civelek M, Ma L, Björkegren JLM, Kumar SR, Tang WHW, Hazen SL, Allayee H · PubMed 33532862

  While most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI. We sought to address the hypothesis that some of the genetic factors which establish atherosclerosis may be distinct from those that predispose to vulnerable plaques and thrombus formation. We carried out a genome-wide association study for MI in the UK Biobank (n∼472 000), followed by a meta-analysis with summary statistics from the CARDIoGRAMplusC4D Consortium (n∼167 000). Multiple independent replication analyses and functional approaches were used to prioritize loci and evaluate positional candidate genes. Eight novel regions were identified for MI at the genome wide significance level, of which effect sizes at six loci were

• Transethnic Meta-Analysis of Genome-Wide Association Studies Identifies Three New Loci and Characterizes Population-Specific Differences for Coronary Artery Disease. - Circulation. Genomic and precision medicine (2021) · Matsunaga H, Ito K, Akiyama M, Takahashi A, Koyama S, Nomura S, Ieki H, Ozaki K, Onouchi Y, Sakaue S, Suna S, Ogishima S, Yamamoto M, Hozawa A, Satoh M, Sasaki M, Yamaji T, Sawada N, Iwasaki M, Tsugane S, Tanaka K, Arisawa K, Ikezaki H, Takashima N, Naito M, Wakai K, Tanaka H, Sakata Y, Morita H, Sakata Y, Matsuda K, Murakami Y, Akazawa H, Kubo M, Kamatani Y, Komuro I · PubMed 32469254

  Genome-wide association studies provided many biological insights into coronary artery disease (CAD), but these studies were mainly performed in Europeans. Genome-wide association studies in diverse populations have the potential to advance our understanding of CAD. We conducted 2 genome-wide association studies for CAD in the Japanese population, which included 12 494 cases and 28 879 controls and 2808 cases and 7261 controls, respectively. Then, we performed transethnic meta-analysis using the results of the coronary artery disease genome-wide replication and meta-analysis plus the coronary artery disease 1000 Genomes meta-analysis with UK Biobank. We then explored the pathophysiological significance of these novel loci and examined the differences in CAD-susceptibility loci between Japa

• Association analyses based on false discovery rate implicate new loci for coronary artery disease. - Nature genetics (2017) · Nelson CP, Goel A, Butterworth AS, Kanoni S, Webb TR, Marouli E, Zeng L, Ntalla I, Lai FY, Hopewell JC, Giannakopoulou O, Jiang T, Hamby SE, Di Angelantonio E, Assimes TL, Bottinger EP, Chambers JC, Clarke R, Palmer CNA, Cubbon RM, Ellinor P, Ermel R, Evangelou E, Franks PW, Grace C, Gu D, Hingorani AD, Howson JMM, Ingelsson E, Kastrati A, Kessler T, Kyriakou T, Lehtimäki T, Lu X, Lu Y, März W, McPherson R, Metspalu A, Pujades-Rodriguez M, Ruusalepp A, Schadt EE, Schmidt AF, Sweeting MJ, Zalloua PA, AlGhalayini K, Keavney BD, Kooner JS, Loos RJF, Patel RS, Rutter MK, Tomaszewski M, Tzoulaki I, Zeggini E, Erdmann J, Dedoussis G, Björkegren JLM, Schunkert H, Farrall M, Danesh J, Samani NJ, Watkins H, Deloukas P · PubMed 28714975

  Genome-wide association studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at 'genome-wide significance' (P < 5 × 10 ) at the time of this analysis, but a much larger number of putative loci at a false discovery rate (FDR) of 5% (refs. 1,2,3,4). Here we leverage an interim release of UK Biobank (UKBB) data to evaluate the validity of the FDR approach. We tested a CAD phenotype inclusive of angina (SOFT; n = 10,801) as well as a stricter definition without angina (HARD; n = 6,482) and selected cases with the former phenotype to conduct a meta-analysis using the two most recent CAD GWAS. This approach identified 13 new loci at genome-wide significance, 12 of which were on our previous list of loci meeting the 5% FDR threshold, thus providing strong support that the remai

• Uncovering myocardial infarction genetic signatures using GWAS exploration in Saudi and European cohorts - Unknown journal (n.d.) · Unknown authors · PubMed 38072966

  ABSTRACT: Genome-wide association studies (GWAS) have yielded significant insights into the genetic architecture of myocardial infarction (MI), although studies in non-European populations are still lacking. Saudi Arabian cohorts offer an opportunity to discover novel genetic variants impacting disease risk due to a high rate of consanguinity. Genome-wide genotyping (GWG), imputation and GWAS followed by meta-analysis were performed based on two independent Saudi Arabian studies comprising 3950 MI patients and 2324 non-MI controls. Meta-analyses were then performed with these two Saudi MI studies and the CardioGRAMplusC4D and UK BioBank GWAS as controls. Meta-analyses of the two Saudi MI studies resulted in 17 SNPs with genome-wide significance. Meta-analyses of all 4 studies revealed 66 l

• Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease - Unknown journal (n.d.) · Unknown authors · PubMed 29212778

  ABSTRACT: Supplemental Digital Content is available in the text. Rationale: Coronary artery disease (CAD) is a complex phenotype driven by genetic and environmental factors. Ninety-seven genetic risk loci have been identified to date, but the identification of additional susceptibility loci might be important to enhance our understanding of the genetic architecture of CAD. Objective: To expand the number of genome-wide significant loci, catalog functional insights, and enhance our understanding of the genetic architecture of CAD. Methods and Results: We performed a genome-wide association study in 34 541 CAD cases and 261 984 controls of UK Biobank resource followed by replication in 88 192 cases and 162 544 controls from CARDIoGRAMplusC4D. We identified 75 loci that replicated and

• Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants - Unknown journal (n.d.) · Unknown authors · PubMed 36474045

  ABSTRACT: The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We priorit

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