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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE244309 | GEO | 2023/10/03

REPOSITORIES: GEO

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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

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

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

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

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.

2015-02-12 | GSE53437 | GEO

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

Project description:Heart failure with preserved ejection fraction (HFpEF) is a complex, heterogeneous disease involving multiple cellular lineages and mechanisms. Here, we aimed to characterize the cellular heterogeneity and potential mechanisms of HFpEF at single-cell resolution.

2023-09-01 | GSE236585 | GEO

Nicotinamide for the treatment of heart failure with preserved ejection fraction

Project description:Heart failure with preserved ejection fraction (HFpEF) is a highly prevalent and intractable form of cardiac decompensation commonly associated with diastolic dysfunction. Here, we show that diastolic dysfunction in patients with HFpEF is associated with a cardiac deficit in nicotinamide adenine dinucleotide (NAD+). Elevating NAD+ by oral supplementation of its precursor, nicotinamide, improved diastolic dysfunction induced by aging (in 2-year-old C57BL/6J mice), hypertension (in Dahl salt-sensitive rats) or cardiometabolic syndrome (in ZSF1 obese rats). Mechanistically, this effect was mediated partly through alleviated systemic comorbidities and enhanced myocardial bioenergetics, as evidenced by cardiac trasncriptome and metabolome analyses. Simultaneously, nicotinamide directly improved cardiomyocyte passive stiffness and calcium-dependent active relaxation through increased deacetylation of titin and the sarcoplasmic reticulum calcium ATPase 2a, respectively. In a long-term human cohort study, high dietary intake of naturally occurring NAD+ precursors was associated with lower blood pressure and reduced risk of cardiac mortality. Collectively, these results suggest NAD+ precursors, and especially nicotinamide, as potential therapeutic agents to treat diastolic dysfunction and HFpEF in humans.

2021-02-11 | GSE163665 | GEO

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

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

| PRJNA800781 | ENA

Nicotinamide for the treatment of heart failure with preserved ejection fraction

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

| PRJNA687024 | ENA

A preclinical rat model of heart failure with preserved ejection fraction with multiple comorbidities

Project description:As patients with heart failure with preserved ejection fraction (HFpEF) present with multiple comorbidities, we hypothesized, that metabolic syndrome in aging animals could lead to the development of diastolic dysfunction and HFpEF. HFpEF is a common complex morbid syndrome for which there are currently little evidence-based therapies. Obesity-prone rats were exposed to high-fat diet and compared to obesity-resistant rats fed with standard chow. Phenotyping of metabolic syndrome, associated with echocardiographic and cardiac hemodynamic measurements, was performed after 4 and 12 months. Blood and myocardial tissue sampling were performed for pathobiological evaluation. High-fat diet in obesity-prone rats elicited metabolic syndrome, characterized by increased body and abdominal fat weights, glucose intolerance and hyperlipidemia, as well as increased left ventricular (LV) systolic pressure (after 12 months). This was associated with LV diastolic dysfunction (assessed by increased LV end-diastolic pressure) and pulmonary hypertension (assessed by increased right ventricular systolic pressure). Echocardiography revealed significant concentric LV hypertrophy, while LV ejection fraction was preserved. LV remodeling was associated with cardiomyocyte hypertrophy, as well as myocardial and perivascular fibrosis. Circulating levels of soluble ST2 markedly increased in rats with HFpEF, while plasma NT-proBNP levels decreased. RNA-sequencing analysis identified clusters of genes implicated in fatty acid metabolism and calcium-dependent contraction as upregulated pathways in the myocardium of rats with HFpEF. High-fat diet during 12 months in obesity-prone rats led to the development of a relevant preclinical model of HFpEF with multiple comorbidities, suitable for investigating novel therapeutic interventions.

2022-02-02 | GSE189190 | GEO

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