Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47695 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SCD_merged.vcf.gz | Vcf | |||
| SCD_merged.vcf.gz.tbi | Vcf |
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Project description:An initial cellular change in the pathogenesis of heart failure is cardiomyocyte hypertrophy, characterized by increased cell size, enhanced protein synthesis and reactivation of fetal genes. In addition to mechanical stresses, several neurohumoral factors have been identified as potent hypertrophic agents, including angiotensin II, endothelin, and catecholamines. We used microarrays to study the gene expression during cardiac hypertrophy. Balb/c mice (6-8w) were treated with TAC, ATII infusion, and myocardial infarction. TAC model: The transverse aorta (TAC) was constricted at the upper left sternal border by ligation with a 7-silk surgical thread and 27-gauge needle, which was removed thereafter. Sham-operated controls underwent an identical procedure without TAC. At 1 week and 1month after the procedure, LV was harvested. Ang II model.: Ang II was dissolved in 0.9% NaCl at concentrations sufficient to allow an infusion rate of 2.0 mg/kg/day, known to produce hypertension and cardiac hypertrophy. Control mice received a vehicle (saline) via an osmotic minipump. At 1 week after the procedure, LV was harvested. MI model: The proximal portion of the left coronary artery was ligated using an 8-0 nylon thread. Myocardial ischemia was confirmed by the discoloration of the heart and typical ECG changes. After 30 min occlusion, the left coronary artery was reperfused by loosening the ligature. In sham-operated mice (SHAM), the pericardium was opened, but the coronary artery was not ligated. At 1 day, 1week, and 1 month after the procedure, LV was harvested.
2011-12-31 | E-GEOD-26671 | biostudies-arrayexpress
Project description:Cardiac hypertrophy with varying degrees of myocardial fibrosis is commonly associated with coronary artery disease (CAD) related sudden cardiac death (SCD), especially in young victims among whom patterns of coronary artery lesions do not entirely appear to explain the cause of SCD. Aim was sto study the genetic background of hypertrophy, with or without fibrosis, among ischemic SCD victims with single vessel CAD
The study population was derived from the Fingesture study, consisting of all autopsy-verified SCDs in Northern Finland between the years 1998 and 2017 (n=5,869).
2023-09-14 | PRJEB47695 | EVA
Project description:Pathological cardiac hypertrophy is unequivocally identified as an ominous escalation of hemodynamically stressful overload, ultimately heighten risk of sudden death as heart failure (HF) ensues. Here, we explored how dysregulated mitochondrial RNA (mtRNA) metabolism remodels mitochondrial bioenergetics and controls hypertrophic-phenotype cardiopathy in mice and humans. Utilizing targeted genetic approaches and in vivo functional imaging, we describe a potent cardiac pro-hypertrophic role for serine arginine protein kinase 3 (SRPK3), which is highly induced in myocardium upon hypertrophic stimuli. Adult extended expression of SRPK3 in cardiomyocytes (CMs) leads to spontaneously concentric hypertrophy and eventuates sudden cardiac death in mice.
2024-03-05 | GSE260494 | GEO
Project description:Premature ventricular contractions (PVCs) are the most prevalent ventricular arrhythmia in adults. High PVC burden can lead to left ventricular (LV) systolic dysfunction, eccentric hypertrophy, and an increased risk of heart failure (HF) and sudden cardiac death (SCD). Deficient angiogenesis is a key determinant in the transition from adaptive to maladaptive cardiac hypertrophy and fibrosis is a risk factor for arrhythmias and SCD. Here, the primary objective was to quantitatively assess the structural remodeling and transcriptional alterations associated with PVC-induced cardiomyopathy (PVC-CM). Canines were implanted with modified pacemakers to reproduce bigeminal PVCs (200-220 ms coupling interval) for 12 weeks. Collagen deposition and interstitial ultrastructure were visualized using light and transmission electron microscopy, respectively, in LV samples. Morphometric studies of pericytes, fibroblasts, myocytes, smooth muscle and endothelial cells were performed using confocal microscopy and quantified with an artificial intelligence-based segmentation analysis and compared using hierarchical statistics. Transcriptional changes were assessed via RNAseq. Although the cardiomyocytes were hypertrophied in PVC-CM LV samples, capillary rarefaction was not observed due to an increase in capillary-to-myocyte ratio. Additionally, thicker blood vessels were more abundant in PVC-CM. Fibroblast-to-myocyte ratio more than doubled, interstitial collagen fibers increased, and the interstitial space thickened in PVC-CM. Transcripts involved in interstitial remodeling, inflammatory response, and alarmins were strongly elevated in PVC-CM. While the angiogenic response meets the metabolic demands of cardiac hypertrophy, upregulated markers of inflammation and cardiomyopathy linked to reactive fibrosis collectively represent an adverse remodeling that heightens the risk of HF and SCD in PVC-CM.
2025-06-25 | GSE296225 | GEO
Project description:Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. Given that Lin28a can bind to diverse mRNA to regulate their abundance and/or translation, we conducted RNA-seq to profile the cardiac transcriptome alteration without Lin28a under pressure overload. It showed that metabolic pathways, including glycolysis and biosynthetic pathway, were remarkedly affected. Thus, our study identifies Lin28a as a crucial regulator of cardiac hypertrophy via its role in metabolic programming.
2019-04-30 | GSE106897 | GEO
Project description:ScRNA-seq was used to investigate the effects of autocrine versus paracrine VEGF-B signaling in the heart using transgenic mouse models. The paracrine model was further investigated in pregnancy-induced cardiac hypertrophy as well as in mice with ligation of the left anterior descending (LAD) coronary artery.
2024-04-19 | GSE261561 | GEO
Project description:Background: Right ventricular (RV) and left ventricular (LV) myocardium differ in their response to pressure-overload hypertrophy (POH). In this report we use microarray and proteomic analyses to identify pathways modulated by LV-, and RV-POH in the immature heart. Methods: Newborn New Zealand White rabbits underwent banding of the descending thoracic aorta (LV-POH; n=6). RV-POH was achieved by banding the pulmonary artery (n=6). Sham–control animals (SC; n=6 each) were sham-manipulated. Following 4 (LV-POH) and 6 weeks (RV-POH) recovery, the hearts were removed and matched sample RNA and proteins were isolated for microarray and proteomic analysis. Results: There was no difference in body weight in RV-, LV-POH vs. SC but there was a significant increase vs. SC in RV (3.2±0.8g vs. 1.2±0.3g; P<0.01) and LV weight (7.08±0.6g vs. 4.02±0.2g; P<0.01). Fractional area change (RV-POH) and shortening fraction (LV-POH) decreased significantly (23±6 vs. 47±6 and 21±4 vs.44±2, respectively, P<0.01). Microarray analysis demonstrated that LV-POH enriched pathways for oxidative phosphorylation, mitochondria energy pathways, actin, ILK, hypoxia, calcium and protein kinase-A signalling. RV-POH enriched pathways for cardiac oxidative phosphorylation. Proteomic analysis revealed 19 proteins were uniquely expressed in LV-POH vs. SC. Functional annotation clustering analysis indicated significant enrichment for the mitochondrion, cellular macromolecular complex assembly and oxidative phosphorylation. RV-POH had 15 uniquely expressed proteins vs. SC. Functional annotation clustering analysis indicated significant enrichment in structural constituents of muscle, cardiac muscle tissue development and calcium handling. Conclusion: Our results identify unique transcript and protein expression profiles in LV, RV-POH and provide new insight into the biological basis of ventricular specific hypertrophy. 3 different conditions: PAB-RV vs. Sham-control RV, PAB-RV [test] vs. PAB-LV [control], AOB-LV vs. Sham-control LV.
2011-06-24 | E-GEOD-30194 | biostudies-arrayexpress
Project description:Transcriptome profiling of naïve and platelet-stimulated monocytes from healthy human subjects separated into two different age groups. Ethical approval was obtained from the Derby Main Research Ethics Committee (REC 06/Q2401/134) and the institutional Research and Development Department (RM61056) at the University of Leicester, UK. Briefly, two groups of 17 healthy Northern European Caucasian males were recruited divided by age (age range 18-40, or 40-65 years). Exclusion criteria comprised any pre-existing illness, pharmacotherapy, or family history of premature coronary artery disease (CAD), cerebrovascular disease, or sudden cardiac death. All subjects were fasted for a minimum of 10 hours and had refrained from consuming caffeine for a minimum of 12 hours prior to blood sampling. Clinical and laboratory data were generated using standard methods in the Departments of Cardiology and Clinical Chemistry, Glenfield Hospital, University of Leicester, UK. Informed consent was obtained from all participants.
2019-02-01 | E-MTAB-5621 | biostudies-arrayexpress
Project description:Genetic variants associated with coronary artery disease in Indians
| PRJNA429566 | ENA