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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [control vs HF]

ABSTRACT: Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [control vs HF]

PROVIDER: PRJNA1003514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25573331.fastq.gz	Fastqsanger.gz
	SRR25573332.fastq.gz	Fastqsanger.gz
	SRR25573333.fastq.gz	Fastqsanger.gz
	SRR25573334.fastq.gz	Fastqsanger.gz
	SRR25573335.fastq.gz	Fastqsanger.gz

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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [control vs HF]

Project description:Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in heart failure with preserved ejection fraction (HFpEF), but the underlying mechanisms remain poorly understood. Here, RNA sequencing identifies Forkhead Box1 (FoxO1) signaling as abnormal in HFpEF hearts. Genetic suppression of FoxO1 alters the intercellular communication between cardiomyocytes and fibroblasts, alleviates abnormal diastolic relaxation, and reduces arrhythmias. Targeted downregulation of FoxO1 in activated fibroblasts reduces cardiac fibrosis, blunts arrhythmogenesis and improves diastolic function in HFpEF. These results not only implicate FoxO1 in arrhythmogenesis and lusitropy but also demonstrate that pro-fibrotic cardiomyocyte-fibroblast communication can be corrected, constituting a novel therapeutic strategy for HFpEF.

2024-11-17 | GSE240401 | GEO

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [scRNA-seq]

2024-11-17 | GSE240403 | GEO

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [6 wks]

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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction

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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [scRNA-seq]

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [scRNA-seq]

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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [6 wks]

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [6 wks]

| PRJNA1003504 | ENA

Characterization of a robust mouse model for heart failure with preserved ejection fraction

Project description:Heart failure with preserved ejection fraction (HFpEF) is a clinical syndrome with multisystem organ dysfunction in which patients develop symptoms of HF as the result of high left ventricular (LV) diastolic pressure Continuous infusion of angiotensin II and phenylephrine (AngII/PE) demonstrates a strong HFpEF phenotype RNAseq data demonstrate activation of pathways leading to myocardial metabolic changes, activation of ECM deposition, microvascular rarefaction, and pressure and volume related myocardial stress

2023-06-07 | GSE221502 | GEO

Canagliflozin regulates ferroptosis to ameliorate heart failure in rats with preserved ejection fraction

Project description:Chronic heart failure (CHF), with whether reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF), is the end-stage of various cardiovascular diseases and severely affects the patients’ lifespan. There has been no effective drugs to improve clinical outcomes for a long time. Sine the recent years, as a hypoglycemic drug, sodium-glucose cotransporter 2 inhibitor (SGLT2i) has aroused great attention due to it’s cardiovascular benefits. However, the underlying mechanisms remain unclear, particularly regarding ferroptosis, a newly defined mechanism of iron-dependent non-apoptotic cell death in heart failure (HF). Here, we discovered and demonstrated that ferroptosis was a key mechanism in rat model of high-salt diet-induced HF, characterized by iron overloading and lipid peroxidation, which was blocked by canagliflozin administration. These findings highlight that targeting ferroptosis serves as a cardioprotective strategy for HF prevention and canagliflozin might display cardiovascular benefits through ferroptosis mitigation.

2022-05-20 | PXD029031 | Pride

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

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-11-17 | GSE240404 | GEO