Key result
ICG-001 administered for 10 days post-myocardial infarction significantly improved left ventricular ejection fraction by 8.4% compared to PBS controls in a rat model.
Why the study?
Does ICG-001 improve ejection fraction in female rats post-myocardial infarction?
Does ICG-001 improve ejection fraction in female rats post-myocardial infarction?
Mean Difference: 8.4
Absolute Event Rate: 54.6% vs 46.2%
p-value: p=0.031
Wnt modulation via ICG-001 offers a promising therapeutic strategy for restoring myocardial tissue and enhancing cardiac function following infarction in a preclinical model.
Hypothesis-generating for Wnt modulation post-MI in rats; leaves open translation to females and clinical use.
The adult mammalian heart has limited capability for self-repair after myocardial infarction. Therefore, therapeutic strategies that improve post-infarct cardiac function are critically needed. The small molecule ICG-001 modulates Wnt signaling and increased the expression of genes beneficial for cardiac regeneration in epicardial cells. Lineage tracing experiments, demonstrated the importance of β-catenin/p300 mediated transcription for epicardial progenitor contribution to the myocardium. Female rats given ICG-001 for 10 days post-occlusion significantly improved ejection fraction by 8.4%, compared to controls (P<0.05). Taken together, Wnt modulation via β-catenin/CBP inhibition offers a promising therapeutic strategy towards restoration of myocardial tissues and an enhancement of cardiac functions following infarction.
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Sasaki et al. (2013) studied Myocardial infarction (n=20). ICG-001 vs. Phosphate-buffered saline (PBS) was evaluated on Left ventricular ejection fraction at 4 weeks post-surgery (MD 8.4%, p=0.031). ICG-001 administered for 10 days post-myocardial infarction significantly improved left ventricular ejection fraction by 8.4% compared to PBS controls in a rat model.
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