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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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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.

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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

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Single-Cell Transcriptomic Profiling of Heart Reveals ANGPTL4 Linking Fibroblasts and Angiogenesis inHeart Failure with Preserved Ejection Fraction [scRNA-seq]

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Nicotinamide for the treatment of heart failure with preserved ejection fraction

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