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Heart Failure Network - Nitrate's Effect on Activity Tolerance in Heart Failure with Preserved Ejection Fraction (HFN NEAT-BioLINCC)

ABSTRACT: Heart Failure Network - Nitrate's Effect on Activity Tolerance in Heart Failure with Preserved Ejection Fraction (HFN NEAT-BioLINCC)

PROVIDER: PRJNA1074922 | ENA |

REPOSITORIES: ENA

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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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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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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. Histone 3 trimethylation at lysine 36 (H3k36me3) - a chromatin signature induced by the histone methyltransferase SETD2 – has shown a strong correlation with changes in gene expression in the human failing heart; yet its role in cardiac disease is poorly understood. The present study investigates the role of SETD2/ H3k36me3 in cHFpEF.

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