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P53-dependent mitochondrial compensation in heart failure with preserved ejection fraction

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

PROVIDER: PRJNA800781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17769958_1.fastq.gz	Fastqsanger.gz
	SRR17769958_2.fastq.gz	Fastqsanger.gz
	SRR17769959_1.fastq.gz	Fastqsanger.gz
	SRR17769959_2.fastq.gz	Fastqsanger.gz
	SRR17769960_1.fastq.gz	Fastqsanger.gz

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Chromatin Remodelers in Cardiometabolic Heart Failure with Preserved Ejection Fraction

Project description:Cardiometabolic heart failure with preserved ejection fraction (cHFpEF) is highly prevalent and associated with a poor outcome. Pathological gene expressions in heart failure are accompanied by changes in active histone marks without major alterations in DNA methylation. Whether chromatin modifications participate to obesity-induced HFpEF is largely unknown. We will investigate whether chromatin marks participate to obesity-induced HFpEF in vivo.

2025-06-05 | GSE289265 | GEO

Circulating CD4+ T cells identify DNA methylation diagnostic signatures in heart failure with preserved ejection fraction

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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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Chromatin Remodelers in Cardiometabolic Heart Failure with Preserved Ejection Fraction

Project description:Chromatin Remodelers in Cardiometabolic Heart Failure with Preserved Ejection Fraction

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

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

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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.

2023-10-03 | GSE244304 | GEO

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

Project description:BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) accounts for 50% of heart failure patients. Clinically, HFpEF prevalence show age and gender biases. Although the majority of HFpEF patients are elderly, there is an emergence of young HFpEF patients. A better understanding of the underlying pathogenic mechanism is urgently needed. Here, we aimed to determine the role of aging in the pathogenesis of HFpEF. METHODS AND RESULTS: HFpEF dietary regimen (HFD + L-NAME) was used to induce HFpEF in wildtype and telomerase RNA knockout mice (mTRG2 and mTRG3), an aging murine model. First, both male and female animals develop HFpEF equally. Second, cardiac wall thickening preceded diastolic dysfunction in all HFpEF animals. Third, accelerated HFpEF onset was observed in mTRG2 (at 6-weeks) and mTRG3 (at 4-weeks) compared to wildtype (8-weeks). Fourth, we demonstrate that mitochondrial respiration transitioned from compensatory state (normal basal yet loss of maximal respiratory capacity) to dysfunction (loss of both basal and maximal respiratory capacity) in a p53 dosage dependent manner. Last, using myocardial-specific p53 knockout animals, we demonstrate that p53 is necessary for the development of HFpEF. CONCLUSIONS: Here we demonstrate that p53 activation is critical for the pathogenesis of HFpEF. We show that short telomere animals exhibit a basal level of p53 activation, mitochondria upregulate mtDNA encoded genes as a mean to compensate for blocked mitochondrial biogenesis, and loss of myocardial p53 prevents HFpEF upon HFD + L-NAME challenge.

2022-07-06 | GSE195482 | GEO

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