ArticleNature communications2025
FoxO3 controls cardiomyocyte proliferation and heart regeneration by regulating Sfrp2 expression in postnatal mice.
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 12 papers.
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Who cites it
12 citing papers in PubMed.
- Targeting FOXO3 for the Management of Heart Failure: Current Evidence and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
- Whole-genome sequencing implicates rare, low-frequency and structural non-coding variation at themedRxiv : the preprint server for health sciences · 2026Article
- SFRP2 drives aerobic glycolysis and tumor progression in ovarian cancer by transcriptional upregulation of PTK2B.Journal of translational medicine · 2026Article
- Inhibiting NLPR3 inflammasome by FOXO3-mediated activation of SIRT2 alleviates myocardial injury in rats.Histology and histopathology · 2026Article
- BK Channels Orchestrate Cardiac Homeostasis Through Mitochondrial Uncoupling Proteins.bioRxiv : the preprint server for biology · 2026Article
- Review
- FTO-Eci1 Axis Mediates Exercise-Induced Cardioprotection in Pressure Overload Mice.Biomolecules · 2026Article
- FoxO3 Activation Alleviates Doxorubicin-Induced Cardiomyopathy by Enhancing Autophagic Flux and Suppressing mTOR/ROS Signalling.Journal of cellular and molecular medicine · 2025Article
- Cardiomyocyte regeneration: lessons from neonatal hearts.Regenerative medicine · 2025Article
- The mechanism of secreted frizzled-related protein 1 in alleviating cardiomyocyte injury and heart failure.Frontiers in cardiovascular medicine · 2025Review
- Exosome-basedRegenerative biomaterials · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
The Forkhead box O3 (FoxO3) transcription factor is crucial to controlling heart growth in adulthood, but its exact role in cardiac repair and regeneration in postnatal mice remains unclear. Here, we show that FoxO3 deficiency promotes cardiomyocyte proliferation in postnatal mice and improves cardiac function in homeostatic adult mice. Moreover, FoxO3 deficiency accelerates heart regeneration following injury in postnatal mice at the regenerative and non-regenerative stages. We reveal that FoxO3 directly promotes the expression of secreted frizzled-related protein 2 (Sfrp2) and suppresses the activation of canonical Wnt/β-catenin signaling during heart regeneration. The increased activation of β-catenin in FoxO3-deficient cardiomyocytes can be blocked by Sfrp2 overexpression. In addition, Sfrp2 overexpression suppressed cardiomyocyte proliferation and heart regeneration in FoxO3-deficient mice. These findings suggest that FoxO3 negatively controls cardiomyocyte proliferation and heart regeneration in postnatal mice at least in part by promoting Sfrp2 expression, which leading to the inactivation of canonical Wnt/β-catenin signaling.
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