rs10455872 - LPA

Magnitude 2.8 · 8 studies on file

Reported associations

• Comprehensive genetic study of the insulin resistance marker TG:HDL-C in the UK Biobank. - Nature genetics (2024) · Oliveri A, Rebernick RJ, Kuppa A, Pant A, Chen Y, Du X, Cushing KC, Bell HN, Raut C, Prabhu P, Chen VL, Halligan BD, Speliotes EK · PubMed 38200128

  Insulin resistance (IR) is a well-established risk factor for metabolic disease. The ratio of triglycerides to high-density lipoprotein cholesterol (TG:HDL-C) is a surrogate marker of IR. We conducted a genome-wide association study of the TG:HDL-C ratio in 402,398 Europeans within the UK Biobank. We identified 369 independent SNPs, of which 114 had a false discovery rate-adjusted P value < 0.05 in other genome-wide studies of IR making them high-confidence IR-associated loci. Seventy-two of these 114 loci have not been previously associated with IR. These 114 loci cluster into five groups upon phenome-wide analysis and are enriched for candidate genes important in insulin signaling, adipocyte physiology and protein metabolism. We created a polygenic-risk score from the high-confidence

• 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

• Genome-Wide Association Study and Identification of a Protective Missense Variant on Lipoprotein(a) Concentration: Protective Missense Variant on Lipoprotein(a) Concentration-Brief Report. - Arteriosclerosis, thrombosis, and vascular biology (2021) · Said MA, Yeung MW, van de Vegte YJ, Benjamins JW, Dullaart RPF, Ruotsalainen S, Ripatti S, Natarajan P, Juarez-Orozco LE, Verweij N, van der Harst P · PubMed 33730874

  [Figure: see text].

• A cross-population atlas of genetic associations for 220 human phenotypes. - Nature genetics (2021) · Sakaue S, Kanai M, Tanigawa Y, Karjalainen J, Kurki M, Koshiba S, Narita A, Konuma T, Yamamoto K, Akiyama M, Ishigaki K, Suzuki A, Suzuki K, Obara W, Yamaji K, Takahashi K, Asai S, Takahashi Y, Suzuki T, Shinozaki N, Yamaguchi H, Minami S, Murayama S, Yoshimori K, Nagayama S, Obata D, Higashiyama M, Masumoto A, Koretsune Y, Ito K, Terao C, Yamauchi T, Komuro I, Kadowaki T, Tamiya G, Yamamoto M, Nakamura Y, Kubo M, Murakami Y, Yamamoto K, Kamatani Y, Palotie A, Rivas MA, Daly MJ, Matsuda K, Okada Y · PubMed 34594039

  Current genome-wide association studies do not yet capture sufficient diversity in populations and scope of phenotypes. To expand an atlas of genetic associations in non-European populations, we conducted 220 deep-phenotype genome-wide association studies (diseases, biomarkers and medication usage) in BioBank Japan (n = 179,000), by incorporating past medical history and text-mining of electronic medical records. Meta-analyses with the UK Biobank and FinnGen (n = 628,000) identified ~5,000 new loci, which improved the resolution of the genomic map of human traits. This atlas elucidated the landscape of pleiotropy as represented by the major histocompatibility complex locus, where we conducted HLA fine-mapping. Finally, we performed statistical decomposition of matrices of phenome-wid

• Genetic Association Analyses Highlight , , and As 3 New Susceptibility Genes Underlying Calcific Aortic Valve Stenosis. - Circulation. Genomic and precision medicine (2020) · Thériault S, Dina C, Messika-Zeitoun D, Le Scouarnec S, Capoulade R, Gaudreault N, Rigade S, Li Z, Simonet F, Lamontagne M, Clavel MA, Arsenault BJ, Boureau AS, Lecointe S, Baron E, Bonnaud S, Karakachoff M, Charpentier E, Fellah I, Roussel JC, Philippe Verhoye J, Baufreton C, Probst V, Roussel R, Redon R, Dagenais F, Pibarot P, Mathieu P, Le Tourneau T, Bossé Y, Schott JJ · PubMed 32141789

  Calcific aortic valve stenosis (CAVS) is a frequent and life-threatening cardiovascular disease for which there is currently no medical treatment available. To date, only 2 genes, and , have been identified as causal for CAVS. We aimed to identify additional susceptibility genes for CAVS. A GWAS (genome-wide association study) meta-analysis of 4 cohorts, totaling 5115 cases and 354 072 controls of European descent, was performed. A TWAS (transcriptome-wide association study) was completed to integrate transcriptomic data from 233 human aortic valves. A series of post-GWAS analyses were performed, including fine-mapping, colocalization, phenome-wide association studies, pathway, and tissue enrichment as well as genetic correlation with cardiovascular traits. In the GWAS meta-analysis, 4 l

• 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

• Genome-wide association study evaluating lipoprotein-associated phospholipase A2 mass and activity at baseline and after rosuvastatin therapy. - Circulation. Cardiovascular genetics (2013) · Chu AY, Guilianini F, Grallert H, Dupuis J, Ballantyne CM, Barratt BJ, Nyberg F, Chasman DI, Ridker PM · PubMed 23118302

  Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is a proinflammatory enzyme bound to low-density lipoprotein cholesterol and other circulating lipoproteins. Two measures of Lp-PLA(2), mass and activity, are associated with increased cardiovascular risk. Data are sparse regarding genetic determinants of Lp-PLA(2) mass and activity, and no prior data are available addressing genetic determinants of statin-induced changes for this proinflammatory biomarker. We performed a genome-wide association study of Lp-PLA(2) mass and activity at baseline and after 12 months of rosuvastatin therapy (20 mg/d) among 6851 participants of European ancestry from the Justification for Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) and performed replication in a meta

• Genetic variants, plasma lipoprotein(a) levels, and risk of cardiovascular morbidity and mortality among two prospective cohorts of type 2 diabetes. - European heart journal (2012) · Qi Q, Workalemahu T, Zhang C, Hu FB, Qi L · PubMed 21900290

  To examine the relations between genetic loci, plasma lipoprotein(a) [Lp(a)] levels, and cardiovascular disease (CVD) risk among diabetic patients and compare with the observations in the general population. In two prospective cohorts of patients with type 2 diabetes (n= 2308) from the Nurses' Health Study and the Health Professional Follow-Up Study, we performed (i) genome-wide association (GWA) scans for plasma Lp(a); (ii) prospective analysis of plasma Lp(a) for CVD risk and mortality; and (iii) genetic association analysis for CVD risk and mortality. Meta-analysis of the two GWA scans yielded 71 single-nucleotide polymorphisms (SNPs) on chromosome 6q associated with plasma Lp(a) levels at a genome-wide significance level (P< 5 × 10(-8)). The SNP rs10455872 in LPA was most strongly ass

Auto-generated from study metadata. AI-synthesised commentary is added when this entry is regenerated through content-service's LLM mode.