ArticleNature communications2025
Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Cardiac fibroblast diversity in HFpEF: states, niches, interorgan drivers and targets.Nature reviews. Cardiology · 2026Review
- A large-scale single-nucleus resource reveals a cardiomyocyte-like fibroblast and stage-specific remodeling across cardiomyopathies.BMC medicine · 2026Article
- Selective loss of Cx40 and conduction abnormalities underlie enhanced atrial fibrillation susceptibility in a HFpEF model in male mice.Physiological reports · 2026Article
- Normal cardiac lymphatics and their mimics.American journal of physiology. Heart and circulatory physiology · 2026Article
- PHLDA1 is a shared diagnostic and key mediator of inflammatory fibrosis in heart and kidney.Frontiers in immunology · 2026Article
- Targeting mTORC2-dependent AKT/FOXO1/RNF125 signaling exploits a therapeutic vulnerability in c-MET-activated and β-catenin-mutated hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
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 male 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 remodeling and cardiomyocyte-fibroblast communication can be corrected, constituting an alternative therapeutic strategy for HFpEF.
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Registered trials
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