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RNA-sequencing of epicardial adipose tissue of heart failure patients with preserved ejection fraction

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE192886 | GEO | 2022/01/05

REPOSITORIES: GEO

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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

RNA-sequencing of epicardial adipose tissue of patients with atrial fibrillation

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2019-08-07 | GSE135445 | GEO

Transcriptomics of cardiac biopsies reveals differences in patients with or without diagnostic parameters for heart failure with preserved ejection fraction

Project description:Heart failure affects 2–3% of adult Western population. Prevalence of heart failure with preserved left ventricular (LV) ejection fraction (HFpEF) increases. Studies suggest HFpEF patients to have altered myocardial structure and functional changes such as incomplete relaxation and increased cardiac stiffness. We hypothesised that patients undergoing elective coronary bypass surgery (CABG) with HFpEF characteristics will show distinctive gene expression compared to patients with normal LV physiology. Myocardial biopsies for mRNA expression analysis were obtained from sixteen patients with LV ejection fraction ≥ 45%. Five out of 16 patients (31%) had echocardiographic characteristics and increased NTproBNP levels indicative of HFpEF and this group was used as HFpEF proxy, while 11 patients had Normal LV physiology. Utilising principal component analysis, the gene expression data clustered into two groups, corresponding to HFpEF proxy and Normal physiology, and 743 differentially expressed genes were identified. The associated top biological functions were cardiac muscle contraction, oxidative phosphorylation, cellular remodelling and matrix organisation. Our results also indicate that upstream regulatory events, including inhibition of transcription factors STAT4, SRF and TP53, and activation of transcription repressors HEY2 and KDM5A, could provide explanatory mechanisms to observed gene expression differences and ultimately cardiac dysfunction in the HFpEF proxy group. <br> Sequencing data from clinical patients fall under GDPR regulations of sharing of personal data and will be made available through EGA-SE.

2019-03-02 | E-MTAB-7454 | biostudies-arrayexpress

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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2024-07-12 | GSE270896 | 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

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

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

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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

Unveiling human proteome signatures of heart failure with preserved ejection

Project description:Heart Failure with preserved ejection fraction (HFpEF) is a major health challenge affecting millions of people worldwide. Moreover, this disease presents multiple etiologies and associated comorbidities, leading to difficulties in diagnosis and limited therapeutic options. HFpEF underlying cellular pathophysiological mechanisms require further investigation. In this study, quantitative proteomic analysis by advanced mass spectrometry (SWATH-MS) was employed to investigate signaling pathways and mechanisms that correlate with HFpEF. Protein expression profiles were analyzed in HFpEF and non-HFpEF human left ventricular myocardium biopsy samples. Functional analysis revealed several proteins that correlated with HFpEF, including proteins associated with mitochondrial dysfunction, oxidative stress reaction, and inflammation. Additionally, proteomic profiles of HFpEF patients with diabetes mellitus indicate reduced mitochondrial oxidative phosphorylation and fatty acid oxidation capacity. Data obtained also reflects the known heterogeneity of HFpEF clinical variables. The proteomic characterization described in this work provides new insights and raises new questions related to HFpEF cellular pathophysiology, paving the way to additional studies focused on the development of novel therapies and diagnosis strategies for HFpEF patients.

2022-11-29 | PXD033876 | Pride

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