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September 28, 2026

FOXC1 knockdown suppresses cardiomyocyte hypertrophy and alleviates mitochondrial dysfunction via the FTO axis in preclinical models.

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Why the study?

The functional role of FOXC1 in cardiac hypertrophy and its impact on cardiomyocyte hypertrophy and mitochondrial dysfunction remain unclear.

Does FOXC1 knockdown reduce hypertrophic responses and mitochondrial dysfunction in models of cardiac hypertrophy?

Population

TAC-induced cardiac hypertrophy mice and Ang II-induced cardiomyocytes (AC16 cells)

Comparison

FOXC1 knockdown using FOXC1 siRNA vs control

Design

Preclinical experimental study

Key result

FOXC1 knockdown suppressed cardiomyocyte hypertrophy and alleviated mitochondrial dysfunction by regulating the FTO axis in preclinical models.

Authors

XKXiao KongXLXuan LiYZYanpeng Zhang

Discussion

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Overview

Hypothesis-generating for FOXC1-FTO targeting in hypertrophy; clinical translation requires prospective human validation.

Key Points

  • To investigate the functional role and underlying mechanisms of FOXC1 in regulating cardiomyocyte hypertrophy and mitochondrial dysfunction in pathological cardiac hypertrophy.
  • Measured FOXC1 expression in transverse aortic constriction (TAC) mouse models and angiotensin II (Ang II)-induced AC16 cardiomyocytes.
  • Transfected cardiomyocytes with FOXC1 siRNA to examine changes in cell surface area, hypertrophic markers (ANP and BNP), oxidative stress, and mitochondrial membrane potential.
  • Evaluated the regulatory relationship between FOXC1 and the transcriptional activity of FTO.
  • FOXC1 expression increased in TAC-induced mouse hearts and Ang II-stimulated cardiomyocytes.
  • FOXC1 knockdown significantly decreased cell surface area, reduced ANP and BNP levels, and improved mitochondrial function by reducing oxidative stress and restoring mitochondrial membrane potential.
  • FOXC1 suppressed the transcriptional activity of FTO, and direct FTO inhibition reversed the protective effects induced by FOXC1 silencing.

Structured PICO

Does FOXC1 knockdown reduce hypertrophic responses and mitochondrial dysfunction in models of cardiac hypertrophy?

P
Population
Transverse aortic constriction (TAC)-induced cardiac hypertrophy mice and angiotensin II (Ang II)-induced cardiomyocytes (AC16 cells)
I
Intervention
FOXC1 knockdown using FOXC1 siRNA
O
Outcome
Hypertrophic responses (ANP and BNP levels, cardiomyocyte surface area) and mitochondrial dysfunction (oxidative stress levels and mitochondrial membrane potential)surrogate

FOXC1 knockdown alleviates cardiomyocyte hypertrophy and mitochondrial dysfunction via the FTO axis, presenting a potential therapeutic target for pathological myocardial hypertrophy.

Cite This Study

Kong et al. (2026) studied Cardiac hypertrophy. FOXC1 knockdown vs. Control was evaluated on Cardiomyocyte hypertrophy and mitochondrial dysfunction. FOXC1 knockdown suppressed cardiomyocyte hypertrophy and alleviated mitochondrial dysfunction by regulating the FTO axis in preclinical models.

synapsesocial.com/papers/6ab9b5927822ec8fc3d907e5https://doi.org/10.14670/hh-25-142
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Also Consider

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

  1. 1FOXF1 ameliorates angiotensin II-induced cardiac fibrosis in cardiac fibroblasts through inhibiting the TGF-β1/Smad3 signaling pathway2020 · 19 citations
  2. 2The Role and Molecular Mechanism of FoxO1 in Mediating Cardiac Hypertrophy2020 · 46 citations
  3. 3Forkhead box O6 (FoxO6) promotes cardiac pathological remodeling and dysfunction by activating Kif15–TGF‐β1 under aggravated afterload2023 · 8 citations
  4. 4Abstract Wed035: Foxe1 Loss of Function Contributes to Adverse Remodeling in the Heart2025
  5. 5Genomic Binding Patterns of Forkhead Box Protein O1 Reveal Its Unique Role in Cardiac Hypertrophy2020 · 21 citations