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October 9, 2025Circulation Research

Abstract Wed035: Foxe1 Loss of Function Contributes to Adverse Remodeling in the Heart

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Key result

Foxe1 functional loss in mice significantly increased cardiac collagen volume fraction compared to wild type (1.2% vs 0.94%, p=0.038), inducing fibrosis and inflammation.

Population

20-week-old tamoxifen-induced Foxe1 deficient mice and isolated mouse cardiac fibroblasts

Comparison

Foxe1 functional loss vs Age-matched wild type mice

Design

Preclinical

Authors

AWAlexander WidiapradjaWest Virginia UniversityHCHeather ConneryWest Virginia UniversityMBMartyn BullockThe University of Sydney

Discussion

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Implication

Loss of Foxe1 function in the heart induces fibrosis and inflammation, highlighting its potential role in preventing adverse cardiac remodeling.

Key Points

  • Foxe1 functional loss leads to increased cardiac fibrosis and inflammation in the heart.
  • Analysis showed collagen volume fraction significantly increased in Foxe1 deficient mice at 1.2% compared to 0.94% in wild types.
  • ChIP-seq analysis indicates Foxe1 binds to genes related to fibrosis and cell motility, suggesting regulatory functions.
  • The study highlights the potential of Foxe1 as a therapeutic target for conditions like heart failure with preserved ejection fraction.

Structured PICO

P
Population
Basic science study using 20-week-old tamoxifen-induced Foxe1 deficient mice and isolated mouse cardiac fibroblasts to evaluate the role of Foxe1 in cardiac fibrosis.
E
Exposure
Foxe1 functional loss (tamoxifen-induced deficiency)
C
Comparator
Age-matched wild type mice
O
Outcome
Cardiac fibrosis (collagen volume fraction) and inflammatory cell infiltrationsurrogate

Main Result

Absolute Event Rate: 1.2% vs 0.94%

p-value: p=0.038

Loss of Foxe1 function in the heart induces fibrosis and inflammation, highlighting its potential role in preventing adverse cardiac remodeling.

Cite This Study

Widiapradja et al. (2025) studied Cardiac fibrosis. Foxe1 functional loss vs. Wild type mice was evaluated on Collagen volume fraction (p=0.038). Foxe1 functional loss in mice significantly increased cardiac collagen volume fraction compared to wild type (1.2% vs 0.94%, p=0.038), inducing fibrosis and inflammation.

synapsesocial.com/papers/68e80eb363e2e2f707877daahttps://doi.org/10.1161/res.137.suppl_1.wed035
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Also Consider

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

  1. 1Postnatal Ablation of Foxm1 from Cardiomyocytes Causes Late Onset Cardiac Hypertrophy and Fibrosis without Exacerbating Pressure Overload-Induced Cardiac Remodeling2012 · 35 citations
  2. 2FOXF1 ameliorates angiotensin II-induced cardiac fibrosis in cardiac fibroblasts through inhibiting the TGF-β1/Smad3 signaling pathway2020 · 19 citations
  3. 3Endothelial Forkhead Box Transcription Factor P1 Regulates Pathological Cardiac Remodeling Through Transforming Growth Factor-β1–Endothelin-1 Signal Pathway2019 · 90 citations
  4. 4Forkhead box O6 (FoxO6) promotes cardiac pathological remodeling and dysfunction by activating Kif15–TGF‐β1 under aggravated afterload2023 · 8 citations
  5. 5Upregulated FoxO1 promotes arrhythmogenesis in mice with heart failure and preserved ejection fraction2025 · 7 citations