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Dysregulation of adipocytokines regulated by hsa-miR-548ay-3p/PPARγ signaling pathway leaded to cardiac fibrosis

ABSTRACT: Cardiac fibrosis is the key to the onset of atrial fibrillation (AF), but the mechanism is not fully understood. Our previous study found that fibrosis-related adipocytokines were dysregulated in epicardial adipose tissue (EAT) from patients with AF. In this study, we explored the factor that induce adipocytokines dysregulation and the mechanism underlying adipocytokines dysregulation-induced cardiac fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE288419 | GEO | 2025/01/30

REPOSITORIES: GEO

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RNA-sequencing of epicardial adipose tissue of patients with atrial fibrillation

Project description:Accumulating studies have suggested that epicardial adipose tissue play an important role in the pathogenesis of atrial fibrillation (AF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that bioactive molecules secreted from EAT, including exosomes carrying non-coding RNAs, may modulate atrial remodeling. The aim of the present study was to investigate the expression profile of mRNAs and ncRNAs in EAT with AF.

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Fibrotic Remodelling of Epicardial Adipose Tissue in Patients with Atrial Fibrillation: Comparative Analyses of Histological Findings and Computed Tomographic Imaging

Project description:Aims: We tested the hypothesis that central-marginal dispersion in adipocyte diameter in epicardial adipose tissue (EAT) would represent fibrotic remodelling of EAT, a crucial state to promote atrial myocardial fibrosis to form a substrate of atrial fibrillation (AF). We also investigated whether the central-marginal EAT density ratio by the analyses of computed tomographic (CT) imaging could predict the central-marginal adipocyte diameter ratio in EAT. Methods and results: Left atrial appendage samples were obtained from 76 consecutive AF patients during cardiovascular surgery. EAT at central area (Central EAT) and that adjacent to atrial myocardium (Marginal EAT) were evaluated. Compared to the Central EAT, the dimeter of adipocytes was smaller, fibrotic remodeling of EAT (EAT fibrosis) was more severe, and the infiltration of CD3-, CD68-, or α-SMA-positive cells were more abundant in the Marginal EAT. EAT fibrosis positively correlated with adipocyte diameter in the Central EAT, while it negatively correlated with that in the Marginal EAT, resulting in the tightly positive correlation between EAT fibrosis and the ratio of central to marginal adipocyte diameter (C/M diameter ratio) (r=0.73, p<0.01). The C/M diameter ratio was greater in patients with persistent AF (PeAF) than in those with paroxysmal AF (PAF) (p<0.01). The CT density in Central EAT and Marginal EAT was measured and their ratio (C/M density ratio) was calculated. The C/M density ratio correlated tightly with the C/M diameter ratio (r=0.69, p<0.01). Conclusion: Our results suggest that C/M adipocyte diameter ratio was associated with fibrotic remodeling of EAT and progression of AF. Our results also suggest that C/M adipocyte diameter ratio could be accurately predicted by the analyses of CT findings noninvasively.

2021-08-25 | GSE154436 | GEO

Differential Expression Profiles and Bioinformatics Analysis of tRNA-derived Small RNAs in Epicardial Adipose Tissue of Patients with Atrial Fibrillation

Project description:Atrial fibrillation (AF) is the most common sustained arrythmia, but the potential molecular indicators involved in structural and electronical remodeling remains to be clarified. Epicardial adipose tissue (EAT), a visceral fat depot surrounding the heart, is increasingly recognized to be metabolically active and has been proposed with an arrthymogenicity nature. It is able to secret a myriad of bioactive molecules, including exosomes carrying tRNA derived small RNAs (tsRNAs). Accumulating findings have suggested that these specific tsRNAs dynamically impact fundamental cellular processes, but there are no studies discovering the association between tsRNAs of EAT and AF, and their interactions and potential signaling pathways remain to be elucidated.

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Transcriptome analysis from human epicardial adipose tissue biopsies analyzed according to postoperative atrial fibrillation occurrence after cardiac surgery

Project description:Introduction: Post-operative atrial fibrillation (POAF) is a frequent complication after cardiac surgery, but its pathophysiology remains incompletely understood. Considering that epicardial adipose tissue (EAT) is in close vicinity with the atrial myocardium, we hypothesized that a specific pre-operative EAT phenotype would be associated to POAF onset following surgery. Methods: Patients undergoing cardiac surgery prospectively enrolled in the POMI-AF cohort between February 2016 and June 2017 were studied. EAT samples were collected at the beginning of surgery. Whole-tissue gene expression patterns and the stromal and vascular fraction (SVF) cellular composition were explored. Patients were followed after surgery by continuous ECG to detect POAF onset. Results: Among the 60 patients included in the cohort, 15 POAF and 15 non-POAF patients were matched based on pre-operative characteristics. Gene set enrichment analysis of transcriptomic data from pre-operative EAT samples revealed 40 enriched biological processes in POAF vs non-POAF patients. Most of these processes were related to cellular immune response. Leukocytes (63±15% of total cells), and more specifically lymphocytes (56±13% of total CD45+ cells), represented the major cell subset in the preoperative EAT SVF, with no quantitative differences between POAF and SR patients (76 [52; 84]% vs 56 [50; 64]%, p=0.22). However, POAF patients presented a significantly higher cytotoxic CD8+/helper CD4+ T lymphocyte ratio than SR patients (respectively, 0.69[0.55; 1.19] vs 0.50 [0.31; 0.54], p=0.03) suggesting a cytotoxic shift prior to surgery. Conclusion: Epicardial fat from patients who develop POAF displays a specific pre-operative transcriptome signature characteristic of cellular immune response and cytotoxic lymphocyte enrichment.

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Rac1-Induced Connective Tissue Growth Factor regulates Connexin 43 and N-Cadherin Expression in Atrial Fibrillation

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2010-02-21 | E-GEOD-14975 | biostudies-arrayexpress

Extracellular vesicles from epicardial fat mediate long-distance heart-brain communication and promote atrial fibrillation associated cognitive impairment (EAT exosomal miRNA-seq and hippocampal mRNA-seq)

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2024-05-01 | GSE240776 | GEO

Transcriptional changes associated with advancing stages of heart failure underlie atrial and ventricular arrhythmogenesis underlie atrial and ventricular arrhythmogenesis

Project description:Heart failure (HF) is a leading cause of mortality and is associated with cardiac remodeling. Vulnerability to atrial fibrillation (AF) has been shown to be greater in the early stages of HF, whereas ventricular tachycardia/fibrillation develop during late stages. Here, we explore changes in gene expression that underlie the differential development of fibrosis and structural alterations that predispose to atrial and ventricular arrhythmias.

2019-01-01 | GSE123823 | GEO

Role of PI3K in Atrial Myopathy: Insights from Transgenic Mouse Models and Identification of a Dysregulated PI3K Lipid Profile in Individuals with Atrial Fibrillation

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2025-01-09 | GSE243115 | GEO

IL-1β sensitizes to atrial fibrillation acting through resident macrophages and caspase-1 expression

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2024-12-16 | GSE284265 | GEO

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2023-12-07 | MSV000093605 | MassIVE

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