99829f01-61af-46bf-84bb-22837c488398 - samples
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ABSTRACT:
PROVIDER: EGAD00001007694 | EGA |
REPOSITORIES: EGA
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Project description:64 left atrial appendages from patients without atrial fibrillation (AF) undergoing cardiac surgery, patients with paroxysmal AF and with persistent AF (~20 per group). Trizol RNA isolation, rRNA depletion, paired transcriptome sequencing on illumina NovaSeq 6000. Provided are FastQ and BAM files. Additional data (e.g. clinical characteristics, RIN values etc.) can be provided upon reasonable request. The same RNA samples (62 out of 64) were used for miRNA sequencing. Results from miRNA seuqencing are stored in the EGA database managed by the same DAC.
| EGAD00001007693 | EGA
Project description:Background: Genomic and experimental studies suggest a role for PITX2 in atrial fibrillation (AF). To assess whether this association is relevant for recurrent AF in patients, we tested whether left atrial PITX2 affects recurrent AF after AF ablation. Methods: mRNA concentrations of PITX2 and its cardiac isoform, PITX2c, were quantified in left atrial appendages (LAA) from patients undergoing thoracoscopic AF ablation, either in whole LAA tissue (n=83) or in LAA cardiomyocytes (n=52), and combined with clinical parameters to predict AF recurrence. Literature suggests bone morphogenetic protein 10 (BMP10) as a PITX2-repressed, atrial-specific, secreted protein. BMP10 plasma concentrations were combined with eleven cardiovascular biomarkers and clinical parameters to predict recurrent AF after catheter ablation in 359 patients. Results: Reduced cardiomyocyte PITX2 concentrations, but not whole LAA tissue PITX2, were associated with AF recurrence after thoracoscopic AF ablation (16% decreased recurrence per 2-(ΔΔCt) increase in PITX2). RNA sequencing, qPCR and Western blotting confirmed BMP10 as one of most PITX2-repressed atrial genes. Left atrial size (hazard ratio per mm increase, HR [95%CI] 1.055 [1.028, 1.082], non-paroxysmal AF (HR 1.672 [1.206, 2.318]) and elevated BMP10 (HR 1.339 [CI 1.159, 1.546] per quartile increase) were predictive of recurrent AF. BMP10 outperformed eleven other cardiovascular biomarkers in predicting recurrent AF. Conclusions: Reduced left atrial cardiomyocyte PITX2 and elevated plasma concentrations of the PITX2-repressed, secreted, atrial protein BMP10 identify patients at risk of recurrent AF after ablation.
2020-06-19 | GSE152181 | GEO
Project description:Atrial fibrillation (AF) is the most prevalent arrhythmia and is strongly associated with stroke, heart failure, and increased mortality. However, the role of T cells in AF pathogenesis remains unclear. In this study, we aimed to characterize the detailed landscape and clonal expansion of T cells using single-cell TCR sequencing, and validate our findings via O-link proteomics in plasma. Analysis of left atrial tissues from eight AF patients identified five CD4+ T cells, six CD8+ T cells, and gamma delta T cells based on canonical gene expression markers. Notably, we observed clonal expansion of resident memory and cytotoxic T cells. CellChat analysis highlighted complement signaling–mediated interactions between T cells and fibroblasts. Furthermore, proteomics in plasma using the Olink platform confirmed enriched complement activation in non-paroxysmal AF compared to paroxysmal AF. These findings suggest that activation of complement pathway between T cells and fibroblasts contributes to atrial remodeling and may serve as a potential therapeutic target for AF.
2026-04-01 | GSE294456 | GEO
Project description:Atrial fibrillation (AF) and heart failure (HF) are mutually reinforcing, and the prognosis for both diseases is poor. Vericiguat is the first oral soluble guanylate cyclase (sGC) stimulator to be approved for the treatment of symptomatic, ejection fraction-reduced chronic heart failure (HFrEF) in adults. It exerts a general therapeutic effect on cardiovascular diseases, with a particular efficacy in the treatment of HF. However, the mechanism of vericiguat treatment of atrial fibrillation remains unclear. The objective of this study was to investigate the potential mechanism of vericiguat in the treatment of atrial fibrillation. A retrospective analysis was conducted to investigate the effects of vericiguat on patients with heart failure and paroxysmal AF. Furthermore, the effects of vericiguat on AF and the degree of myocardial fibrosis in rat AF models and cells were observed. It was found that vericiguat can control the recurrence of AF in clinical studies and can control the fibrosis of AF rats in vivo and in vitro experiments. RNA-Seq sequencing revealed that the TGF-β1/Smad pathway in cells treated with vericiguat was significantly enriched. In vitro validation demonstrated that the anti-fibrotic effect of Vericiguat was weakened by the TGF-β1/Smad pathway when Protein Kinase G (PKG) was knocked down. The findings indicate that vericiguat can inhibit myocardial fibroblast activation and collagen synthesis via the TGF-β1/Smad pathway, thereby exerting a controlling effect on the recurrence of atrial fibrillation.
2025-07-23 | GSE278356 | GEO
Project description:Atrial fibrillation (AF) is the most common heart arrhythmia disease. The greatest risk of atrial fibrillation is stroke, and stroke caused by valvular heart disease with atrial fibrillation (AF-VHD) is more serious. the development mechanism from VHD to AF-VHD is not yet clear. The research on expression profiles of lncRNA and mRNA is helpful to explore molecular mechanism in patients with valvular heart disease who develop atrial fibrillation.
2018-04-12 | GSE113013 | GEO
Project description:Atrial fibrillation (AF) is the most common persistent arrhythmia that affect 1–2% of the general population. People with AF display an array of complications cardiogenic stroke and systemic embolism caused by hemodynamic instability and blood hypercoagulability in clinical practice. However, it’s still unclear whether and how ubiquitylated proteins react to AF in the left atrial appendage of patients with AF and valvular heart disease. This theory focuses on the changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease. We firstly widely analysis the proteins ubiquitination in patients with atrial fibrillation.
2021-12-24 | PXD030397 | Pride
Project description:The cause of atrial fibrillation (AF) is unclear and is associated with organic heart disease, pre-excitation syndrome, and other underlying conditions. Medications may also cause AF, such as chemotherapeutic agents. Crizotinib is used as a multi-target protein kinase inhibitor in the treat-ment of non-small cell lung cancer. The most common adverse events with crizotinib are nausea, diarrhoea and vomiting. There are also side effects such as hepatotoxicity, interstitial pneumonitis, prolonged QT interval, and bradycardia. Here, we report a case of crizotinib-induced AF. For the first time, we used peripheral blood mononuclear cells before and after the onset of paroxysmal AF for single-cell sequencing analysis with the aim of determining the mechanism of AF. The single-cell sequencing results and retrospective study showed that monocytes were the most dynamic cell type in the peripheral blood at the onset of AF and increasing proportion of monocytes is an important feature of atrial fibrillation. Meanwhile, retrospective studies have also shown that a higher level of inflammation is a characteristic of patients with AF. Monocyte-mediated adipogenesis-related sig-naling pathway, GALECTIN signaling, and chemokine overexpression were characteristic of pe-ripheral blood mononuclear cells at the onset of AF. At the same time, we found an elevated level of inflammation and an elevated red cell distribution width (RDW) in this patient. These clinical findings corroborate each other with the results of the single-cell analysis, suggesting that inflam-mation is a very important feature in the development of AF.
2024-01-30 | GSE254133 | GEO
Project description:Atrial fibrillation (AF) is the most common irregular heart rhythm which influence approximately 1–2% of the general population. As a potential factor for ischemic stroke, AF could also cause heart failure. The mechanisms behind AF pathogenesis are complex and remains elusive. As a new category of non-coding RNAs (ncRNAs), circular RNAs (circRNAs) have been known as the key of developmental processes, regulation of cell function, pathogenesis of heart diseases and pathological responses which could provide novel sight into the pathogenesis of AF. circRNAs function as modulators of microRNAs in cardiac disease. To investigate the regulatory mechanism of circRNA in atrial fibrillation, especially the complex interactions among circRNA, microRNA and mRNA, we collected the heart tissues from three AF patients and three healthy controls and profiled their circRNA expressions with circRNA Microarray. The differentially expressed circRNAs were identified and the biological functions of their interaction microRNAs and mRNAs were analyzed. Our results provided novel insights of the circRNA roles in atrial fibrillation and proposed highly possible interaction mechanisms among circRNAs, microRNAs and mRNAs.
2019-04-06 | GSE129409 | GEO
Project description:<p>Background. Atrial fibrillation (AF), the most common cardiac arrhythmia worldwide, carries a high risk of severe complications. Patients diagnosed with paroxysmal atrial fibrillation (PAF) may progress to persistent atrial fibrillation (PerAF) following a period. We aimed to identify metabolites associated with PerAF using machine learning (ML), and predict the probability of PAF progressing to PerAF, enabling the adjustment of subsequent treatments in clinical practice.</p><p>Methods. We enrolled AF patients without any anticoagulant therapy within the last 7 days between July 2020 and July 2022 in two centers in China. Targeted metabolomic profiling was performed on patient’s plasma. Differential metabolites and clinical features were identified through univariate and multivariate analyses. Patients were divided into discovery and validation cohorts (70%:30%). Four ML models (logistic regression, random forest, XGBoost, and LightGBM) were developed for PerAF prediction. Model predictive performance was measured mainly by AUC.</p><p>Results. One hundred patients (65 PerAF, 35 PAF) were enrolled. Eight metabolites (kynurenine, N-Acetylaspartic acid, glyceric acid, adipic acid, citramalic acid, malic acid, isocitric acid, and oxoglutaric acid) and two clinical features (NT-proBNP and uric acid) had significant associations with PerAF. Pathway enrichment analysis highlighted alterations in the citrate cycle and glyoxylate/dicarboxylate metabolism. XGBoost was chosen for establishing the final model, since its predictive performance outperformed that of other algorithms. The model based on clinical parameters, metabolites, and demographics achieved the highest AUC in discovery cohort (0.751 [95% CI 0.631~0.867]) and validation cohort (0.985 [95% CI 0.940~1.000]). A simplified model with three features (NT-proBNP, citramalic acid, and uric acid) retained robust performance.</p><p>Conclusions. This study shows strengths in identifying eight PerAF-related metabolites via targeted metabolomics and ML, and developing accurate predictive models (including a simplified, clinically feasible model) to guide early PerAF intervention. Future directions include large-scale multi-center validation, incorporating more confounders, and using multiple platforms to deeply explore AF-related metabolic alterations.</p>
2026-07-03 | MTBLS13136 | MetaboLights
Project description:Atrial fibrillation (AF) is often a progressive cardiac arrhythmia that increases the risk of hospitalization and adverse cardiovascular events. There is a clear demand for more inclusive and large-scale approaches to understand the molecular drivers responsible for AF, as well as the fundamental mechanisms governing the transition from paroxysmal to persistent and permanent forms. We aimed to create a molecular map of AF and find the distinct genetic programs underlying cell type-specific atrial remodeling and AF progression. We used a sheep model of long-standing, tachypacing-induced AF, sampled right and left atrial tissue and isolated cardiomyocytes from control, intermediate (transition) and late time points during AF progression, and performed transcriptomic and proteome profiling. We have merged all these layers of information into a meaningful 3-component space in which we explored the genes and proteins detected and their common patterns of expression. Our data-driven analysis points at extracellular matrix remodeling, inflammation, ion channel, myofibril structure, mitochondrial complexes and chromatin remodeling as hallmarks of AF progression. Most important, we prove that these changes occur at early transitional stages of the disease, but not at later stages, and that the left atrium undergoes significantly more profound changes than the right atrium in its expression program. The pattern of dynamic changes in gene and protein expression correspond closely with the electrical and structural remodeling demonstrated previously in the sheep and in humans. The results provide novel insight into the dynamics of gene and protein expression changes that underlie AF-induced atrial remodeling and that make the arrhythmia become more stable and long lasting.
2021-01-08 | PXD015637 | Pride