Key result
Selective disruption of the Ndufs4 gene in the mouse heart led to a severe decrease in left ventricular ejection fraction (26.8% vs 67.1%, p<0.001) and hypertrophic cardiomyopathy.
Population
Heart-specific Ndufs4-null mice and control mice on a C57Bl/6 background, aged 8-24 weeks.
Comparison
Heart-specific Ndufs4 gene ablation causing mild… vs Control mice (Ndufs4+/LoxP or Ndufs4LoxP/LoxP)
Design
Preclinical
Follow-up
8-24 weeks of age
Authors
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Mitochondrial complex I disruption may drive hypertrophic cardiomyopathy in mice; leaves open relevance to human disease mechanisms or therapies.
Absolute Event Rate: 26.8% vs 67.1%
p-value: p=<0.001
Diminished mitochondrial complex I activity in the heart is sufficient to drive severe hypertrophic cardiomyopathy independently of alterations in mitochondrial hydrogen peroxide levels or oxidative damage.
Chouchani et al. (2014) studied Hypertrophic cardiomyopathy. Heart-specific Ndufs4 gene ablation vs. Control mice was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.001). Selective disruption of the Ndufs4 gene in the mouse heart led to a severe decrease in left ventricular ejection fraction (26.8% vs 67.1%, p<0.001) and hypertrophic cardiomyopathy.
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