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RNA-sequencing of epicardial adipose tissue of heart failure patients with preserved ejection fraction

ABSTRACT: RNA-sequencing of epicardial adipose tissue of heart failure patients with preserved ejection fraction

PROVIDER: PRJNA793683 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17401922_1.fastq.gz	Fastqsanger.gz
	SRR17401922_2.fastq.gz	Fastqsanger.gz
	SRR17401923_1.fastq.gz	Fastqsanger.gz
	SRR17401923_2.fastq.gz	Fastqsanger.gz
	SRR17401924_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing of epicardial adipose tissue of heart failure patients with preserved ejection fraction

Project description:Recent studies have suggested that epicardial adipose tissue (EAT) play an important role in the pathogenesis of heart failure with preserved ejection fraction (HFpEF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that molecules secreted from EAT, including exosomes carrying non-coding RNAs (ncRNAs), may participate in the development of HFpEF. The aim of the present study was to investigate the expression profile of mRNAs and ncRNAs in EAT with HFpEF.

2022-01-05 | GSE192886 | GEO

Proteomics of epicardial adipose tissue in heart failure patients with preserved ejection fraction

Project description:Background: Heart failure with preserved ejection fraction (HFpEF) has become a major public health problem with a morbidity and mortality similar to heart failure with reduced ejection fraction (HFrEF). Recently, it has been proved epicardial adipose tissue (EAT) played an important role in the pathogenesis of HFpEF, however the underlying mechanisms are not yet fully elucidated. This study attempted to describe comprehensive proteomic analysis of EAT in HFpEF patients and non-HF patients as controls, and identify local candidate molecules characterizing EAT in HFpEF patients. EAT samples were collected from patients undergoing heart surgery in two groups. Proteins was identified in liquid chromatography-tandem mass spectrometry (LC-MS/MS) experiments. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was conducted and protein-protein interaction network was constructed with Cytoscape software. A total of 2416 proteins were identified in LC-MS/MS experiments and 2349 proteins were quantified. Amongst them, totally 96 significant proteins (including 71 upregulated proteins in abundance and 25 downregulated proteins) were differently expressed between HFpEF and non-HF group. GO-enrichment, KEGG pathway analysis and interaction network construction showed these differentially expressed proteins were predominantly involved in HFpEF-related processes including lipid metabolic disorder, inflammation and mitochondrial dysfunction including FABP5, CD36, CFB, ADSL, POSTN, TRAP1 et al., which might contribute to the pathogenesis of HFpEF. In conclusion, this is the first demonstration to describe the parts of EAT proteome in HFpEF patients. Our findings provide a comprehensive understanding for linking EAT to the pathogenesis of HFpEF, which may offer new insights into the treatment of HFpEF targeting on EAT.

2023-01-30 | PXD028158 | Pride

Heart Failure with Preserved Ejection Fraction - Mouse Heart and Lung Tissue & Comorbidities

Project description:FASILOX analysis of heart and lung tissue form mice with heart failure with preserved ejection fraction and several comorbidities.

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Circulating microRNAs are candidate markers of heart failure and differentiate between heart failure with reduced vs preserved left ventricular ejection fraction.

Project description:In this study, we compared the expression profiles of circulating miRNAs in blood samples from controls and patients with heart ailment. Subject with no past history of heart failure/disease are considered as controls. The patients were classified according to the percentage of left ventricular ejection fraction. Patients were grouped as heart failure with reduced (hfREF) and preserved (hfPEF) left ventricular ejection fraction. Employing miRNA microarray, we identified 'signature miRNAs' in peripheral blood samples that distinguished Heart failure from the non-heart failure controls, as well as those of hfREF and hfPEF groups.

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Myeloid Cell Derived IL1b Contributes to Pulmonary Vascular Remodeling in Heart Failure with Preserved Ejection Fraction

Project description:Goals and objectives of this study were to determine by bulk RNA-sequencing transcriptomic changes that occur in the lungs of a murine model of heart failure with preserved ejection fraction caused by administration of high fat diet and eNOS inhibitor L-NAME.

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Nicotinamide for the treatment of heart failure with preserved ejection fraction

Project description:Nicotinamide for the treatment of heart failure with preserved ejection fraction

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p53-dependent mitochondrial compensation in heart failure with preserved ejection fraction

Project description:p53-dependent mitochondrial compensation in heart failure with preserved ejection fraction

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Molecular and Cellular Mechanisms of Heart Failure With Preserved Ejection Fraction

Project description:To understand the cellular mechanisms of heart failure with preserved ejection fraction (HFpEF), We investigated the functional outcome and the underlying mechanisms from concurrent mechanic and metabolic stresses in the heart by applying transverse aortic constriction (TAC) in lean C57Bl/6J (HFrEF phenotype) or obese/diabetic B6.Cg-Lepob/J (ob/ob) mice (HFpEF phenotype) followed by single-nuclei RNA-seq (snRNA-seq) and targeted manipulation of a top ranked signaling pathway (glucagon receptor signaling) differentially affected in the two experimental cohorts.

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Myeloid Cell Derived IL1b Contributes to Pulmonary Vascular Remodeling in Heart Failure with Preserved Ejection Fraction

Project description:Goals and objectives of this study were to determine on a single-cell level transcriptomic changes that occur in the lungs of a murine model of heart failure with preserved ejection fraction caused by administration of high fat diet and eNOS inhibitor L-NAME.

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Eicosanoid and Eicosanoid-Related Inflammatory Mediators and Exercise Intolerance in Heart Failure with Preserved Ejection Fraction

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