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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE240404 | GEO | 2024/11/17

REPOSITORIES: GEO

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Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [6 wks]

Project description:Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in heart failure with preserved ejection fraction (HFpEF), but the underlying mechanisms remain poorly understood. Here, RNA sequencing identifies Forkhead Box1 (FoxO1) signaling as abnormal in HFpEF hearts. Genetic suppression of FoxO1 alters the intercellular communication between cardiomyocytes and fibroblasts, alleviates abnormal diastolic relaxation, and reduces arrhythmias. Targeted downregulation of FoxO1 in activated fibroblasts reduces cardiac fibrosis, blunts arrhythmogenesis and improves diastolic function in HFpEF. These results not only implicate FoxO1 in arrhythmogenesis and lusitropy but also demonstrate that pro-fibrotic cardiomyocyte-fibroblast communication can be corrected, constituting a novel therapeutic strategy for HFpEF.

2024-11-17 | GSE240400 | GEO

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [scRNA-seq]

2024-11-17 | GSE240403 | GEO

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [control vs HF]

2024-11-17 | GSE240401 | GEO

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction

| PRJNA1003518 | ENA

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [6 wks]

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [6 wks]

| PRJNA1003504 | ENA

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [scRNA-seq]

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [scRNA-seq]

| PRJNA1003523 | ENA

Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [control vs HF]

Project description:Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction [control vs HF]

| PRJNA1003514 | ENA

Heart failure with preserved ejection fraction.

Project description:Heart failure with preserved ejection fraction (HFpEF) represents a heterogeneous collection of conditions that are unified by the presence of a left ventricular ejection fraction ≥50%, evidence of impaired diastolic function and elevated natriuretic peptide levels, all within the context of typical heart failure signs and symptoms. However, while HFpEF is steadily becoming the predominant form of heart failure, disease-modifying treatment options for this population remain sparse. This review provides an overview of the diagnosis, management and prevention of HFpEF for general physicians.

| S-EPMC6334030 | biostudies-literature

Seipin Knockout Mice Develop Heart Failure With Preserved Ejection Fraction.

Project description:The lean diabetic patients with heart failure with preserved ejection fraction (HFpEF) in Asia suffer from adverse clinical outcomes and poor life quality. The suitable animal models are urgently needed for mechanistic study and therapeutic innovations. Our study reports that lipodystrophic mice with seipin depletion are lean, diabetic, and recapitulate major manifestations of clinical HFpEF, thereby clarifying that lean diabetes per se may produce HFpEF characteristics. We further demonstrate that increased cardiac titin phosphorylation and reactive interstitial fibrosis associated with neutrophil extracellular traps lead to left ventricular stiffness and suggest that both pathways may be potential therapeutic targets in Asian HFpEF patients.

| S-EPMC6939002 | biostudies-literature

Managing heart failure with preserved ejection fraction.

Project description:Heart failure with preserved ejection fraction (HFpEF) is increasing in prevalence as the general population ages. Poorly managed heart failure symptoms of decompensated HFpEF is one of the most common reasons for prolonged hospital admission. The high rate of morbidity and mortality associated with HFpEF is compounded by a poor understanding of the underpinning pathophysiology. Randomized controlled trials have so far been unable to identify an evidence base for reducing morbidity and mortality in patients with HFpEF, although there is some evidence to support quality of life (QOL) improvement. In this review, we described the recent advances on the pathophysiological understanding of HFpEF, the current and emerging treatment strategies, and what this may mean for individual patients. Potential treatments for HFpEF were divided into their relative management strategies and the current evidence assessed for effect on HFpEF mortality, hospital admission frequency, and QOL improvement. Overall, the understanding of HFpEF pathophysiology is improving and has been made a priority in identifying potential therapeutic targets. There is growing evidence that patients with ejection fractions (EF) of less than 60% may obtain a mortality benefit from ACE-inhibitors, angiotensin-neprilysin inhibitors, Angiotensin Receptor Blockers, and Mineralocorticoid Receptor Antagonists. However, this covers only a small proportion of the HFpEF spectrum. Therefore, currently there are no universal treatment strategies recommended for HFpEF, and management should focus on an individualised approach and this should take into account the comorbidities of each patient.

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