What does this research mean for the field?

Upregulation of FoxO1 promotes arrhythmogenesis and diastolic dysfunction in HFpEF, and its targeted suppression reduces arrhythmias by improving cardiac fibrosis and cardiomyocyte-fibroblast communication. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 30, 2025Nature CommunicationsOpen Access

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

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Why the study?

Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in HFpEF, but the underlying mechanisms remain poorly understood.

Does genetic suppression of FoxO1 reduce arrhythmias and improve diastolic function in a mouse model of HFpEF?

Population

Male mice with HFpEF

Comparison

Genetic suppression or targeted downregulation of FoxO1 vs control

Design

Preclinical animal study

Authors

TMThássio MesquitaElectrophysiology RMRodrigo Miguel‐dos‐SantosCedars-Sinai Medical Center WLWeixin LiuElectrophysiology

Discussion

Member takes

Overview

No immediate clinical implications in HFpEF; hypothesis-generating for FoxO1 targeting in fibrosis.

Structured PICO

Does genetic suppression of FoxO1 reduce arrhythmias and improve diastolic function in a mouse model of HFpEF?

Population

Male mice with heart failure and preserved ejection fraction (HFpEF)

Intervention

Genetic suppression of FoxO1 (including targeted downregulation in activated fibroblasts)

Outcome

Arrhythmogenesis, cardiac fibrosis, and diastolic functionsurrogate

Targeting FoxO1 signaling reduces cardiac fibrosis and arrhythmogenesis in a mouse model of HFpEF, suggesting a potential novel therapeutic strategy.

Cite This Study

Mesquita et al. (2025) studied this question.

synapsesocial.com/papers/6a1bdf3bc97d63156a5f090b https://doi.org/10.1038/s41467-025-56186-1

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January 30, 2025Nature CommunicationsOpen Access

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

View Full Paper

Ask AI

Bookmark

Why the study?

Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in HFpEF, but the underlying mechanisms remain poorly understood.

Does genetic suppression of FoxO1 reduce arrhythmias and improve diastolic function in a mouse model of HFpEF?

Population

Male mice with HFpEF

Comparison

Genetic suppression or targeted downregulation of FoxO1 vs control

Design

Preclinical animal study

Authors

TMThássio MesquitaElectrophysiology RMRodrigo Miguel‐dos‐SantosCedars-Sinai Medical Center WLWeixin LiuElectrophysiology

Discussion

Member takes

Overview

No immediate clinical implications in HFpEF; hypothesis-generating for FoxO1 targeting in fibrosis.

Structured PICO

Does genetic suppression of FoxO1 reduce arrhythmias and improve diastolic function in a mouse model of HFpEF?

Population

Male mice with heart failure and preserved ejection fraction (HFpEF)

Intervention

Genetic suppression of FoxO1 (including targeted downregulation in activated fibroblasts)

Outcome

Arrhythmogenesis, cardiac fibrosis, and diastolic functionsurrogate

Targeting FoxO1 signaling reduces cardiac fibrosis and arrhythmogenesis in a mouse model of HFpEF, suggesting a potential novel therapeutic strategy.

Cite This Study

Mesquita et al. (2025) studied this question.

synapsesocial.com/papers/6a1bdf3bc97d63156a5f090b https://doi.org/10.1038/s41467-025-56186-1

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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