ApoC3 overexpression exacerbated ischemic heart failure in mice following myocardial infarction, significantly reducing ejection fraction to 18% compared to 27% in wild-type mice.
Does ApoC3 modulation affect the severity of ischemic heart failure in animal models?
ApoC3 drives adverse cardiac remodeling in ischemic heart failure, highlighting its potential as a therapeutic target.
Absolute Event Rate: 18% vs 27%
p-value: p=<0.001
ApoC3 overexpression could activate cardiac TLR2/NF-κB to trigger the inflammation, oxidation, and apoptosis pathways, finally aggravating IHF in mice. Inactivation of ApoC3 could significantly alleviate IHF in hamsters.
Han et al. (2026) studied Ischemic heart failure (n=189). ApoC3 overexpression (ApoC3 Tg) vs. Wild-type (WT) was evaluated on Ejection fraction (EF) at 4 weeks post-myocardial infarction (p=<0.001). ApoC3 overexpression exacerbated ischemic heart failure in mice following myocardial infarction, significantly reducing ejection fraction to 18% compared to 27% in wild-type mice.