Genome wide association study for early onset coronary disease and related phenotypes (ADVANCE)
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ABSTRACT:
PROVIDER: PRJNA76503 | ENA |
REPOSITORIES: ENA
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Project description:<p>ADVANCE (Atherosclerotic Disease, VAscular functioN, and genetiC Epidemiology) is a large epidemiological study of genetic and non-genetic determinants of coronary artery disease (CAD) that started in 2000 as a collaborative effort between researchers at Stanford University and Kaiser Permanente of Northern California. The overarching goal of the study is to improve our ability to prevent, diagnose and treat CAD. The initial study included recruitment of over 3600 subjects (including 1873 subjects with incident clinically significant coronary disease and 1745 control subjects) from multiple race/ethnic backgrounds. A subset of ~ 500 subjects with very early onset coronary disease (men < 45 and women < 55) and ~ 500 similar aged controls were genotyped using the Illumina 550K platform as part of an NIH funded effort within the STAMPEED consortium.</p>
| phs000423.v1.p1 | EGA
Project description:Genome wide association study for early onset coronary disease and related phenotypes (ADVANCE)
| PRJNA76505 | ENA
Project description:The clinical and pathological features of early-onset colorectal cancer (EOCRC) differ from those of late-onset colorectal cancer (LOCRC). Our research aims to thoroughly elucidate the distinctions between them by analyzing clinical prognosis, metastatic patterns, gene expression, and genomic mutation profiles. Our deliberation will uncover latent strategies for personalized therapeutic of both EOCRC and LOCRC.
| 92169 | ecrin-mdr-crc
Project description:eMERGE-I Genome Wide Association Studies of Network Phenotypes
| PRJNA75857 | ENA
Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.
2022-03-04 | PXD008852 | Pride
Project description:Due to the insidious onset and the difficulty to diagnose and intervene, it is particularly important to find the diagnostic markers of diabetic coronary microcirculation disorder (CMD) and therapeutic targets. Circulating exosomes, as endogenous exosomes derived from multiple tissue cells, mediate communication between cells and tissues, may serve as a key point for future diagnosis, prognosis and personalized treatment of CMD in diabetes. Therefore, we isolated serum exosomes from patients with diabetes, as well as patients with CMD or coronary artery disease (CAD) respectively. We explored the differences in characteristics between three circulating exosomes.
2023-09-15 | GSE234464 | GEO
Project description:Genome-wide association studies (GWAS) have identified hundreds of genetic risk loci for coronary artery disease (CAD). However, non-European populations are underrepresented in coronary artery disease (CAD). However, non-European populations are underrepresented in GWAS and the causal gene-regulatory mechanisms of these risk loci during atherosclerosis remain unclear. We incorporated local ancestry and haplotype information to identify quantitative trait loci (QTL) for gene expression and splicing in coronary arteries obtained from 138 ancestrally diverse Americans.
2023-11-14 | GSE225650 | GEO
Project description:We developed a coronary plaque sampling approach that could be applied broadly in live patients with coronary artery disease (CAD) to obtain molecular and cellular insights into human coronary atherosclerosis. Our approach combined RNA retrieval directly from balloons used in percutaneous coronary interventions (PCI) and inexpensive, low-input RNA-Seq using SMART-seq. We generated SMART-Seq libraries from coronary samples from 27 patients. Of the 27 patients, 13 were confirmed to have stable CAD (sCAD) and 14 confirmed to have been performed on lesions causing acute coronary syndrome (ACS). We applied CIBERSORTx to analyze the SMART-seq data from each of the 27 samples. We found fibroblasts and fibromyoctes were enriched, while smooth muscle cells were reduced, in samples from ACS compared with sCAD patients. We identified 371 genes as significantly differential expressed (q<0.05) between sCAD and ACS patients.
2023-07-10 | GSE236610 | GEO
Project description:Rationale: Circular RNAs are pervasively expressed in highly diverged eukaryotes. Circular RNAs are more stable in body fluids, however, the link between circular RNA and onset of atrial fibrillation has never been investigated. Objective: To identify plasma circular RNAs for diagnosing onset of atrial fibrillation after the cardiac surgery. Methods and Results: Plasma circular RNAs expression was investigated in participants underwent isolated off-pump coronary artery bypass grafting. First, we used microarray to screen 15 circular RNAs in 30 plasma samples for diagnosing new onset of atrial fibrillation. Quantitative polymerase chain reaction assay was then applied to evaluate the expression of selected circular RNAs. Hsa_circRNA_025016 was upregulated in patients with onset of atrial fibrillation, with a high diagnostic accuracy by area under the receiver operating characteristic curve. The satisfactory diagnostic performance of hsa_circRNA_025016 persisted in validation cohort. Kyoto Encyclopedia of Genes and Genomes biological pathway analysis indicated that hsa_circ_025016 could participate in melanogenesis, insulin secretion, and thyroid hormone signaling pathway. There was a positive correlation between hsa_circ_025016 and fast blood glucose in both cohorts. Conclusions: Hsa_circ_025016 is a novel biomarker of onset of atrial fibrillation after isolated off-pump coronary artery bypass grafting.
2017-04-07 | GSE97455 | GEO
Project description:Coronary artery disease (CAD) is a complex inflammatory disease of the vessel wall and often leads to myocardial infarction. Genome-wide association studies (GWAS) have now identified over 200 genetic loci associated with CAD. The majority of CAD-associated variants are located in noncoding regions of the genome, many of which are predicted to regulate chromatin accessibility and gene expression. In this study, we performed ATAC-seq in human coronary artery patient samples to identify novel chromatin accessibility QTLs (caQTLs) and gain additional insights into CAD regulatory mechanisms in vivo.
2022-01-24 | GSE188422 | GEO