Key result
Icosapent ethyl improves post-MI survival and limits adverse cardiac remodeling via myeloid GPR120 signaling.
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Why the study?
The effects of icosapent ethyl on post-myocardial infarction cardiac remodeling and the underlying cellular mechanisms remain incompletely understood.
Does icosapent ethyl improve post-myocardial infarction cardiac remodeling and survival in a murine model?
Does icosapent ethyl improve post-myocardial infarction cardiac remodeling and survival in a murine model?
Icosapent ethyl improves post-myocardial infarction cardiac remodeling and survival in mice by activating GPR120 signaling in myeloid cells and suppressing proinflammatory cell recruitment.
Icosapent ethyl, a high-purity ethyl ester of eicosapentaenoic acid (EPA), has demonstrated cardiovascular benefit in clinical trials; however, its effects on post-myocardial infarction (MI) cardiac remodeling and the underlying cellular mechanisms remain incompletely understood. Here, we investigated the role of icosapent ethyl in regulating post-MI remodeling using a murine MI model with myeloid-specific deletion of the omega-3 fatty acid receptor GPR120. Icosapent ethyl treatment significantly improved survival, preserved left ventricular systolic function, attenuated adverse ventricular remodeling and interstitial fibrosis, reduced cardiomyocyte apoptosis, and preserved myocardial microvascular density after MI. The protective effects of icosapent ethyl were markedly attenuated in myeloid GPR120-deficient mice. Mechanistically, icosapent ethyl activated GPR120 signaling in myeloid cells, suppressed CXCL10 expression, and reduced recruitment of proinflammatory CXCR3
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Liu et al. (2026) studied Myocardial Infarction. Icosapent ethyl was evaluated on Post-MI cardiac remodeling, survival, and left ventricular systolic function. Icosapent ethyl treatment improved survival and attenuated adverse cardiac remodeling after myocardial infarction in mice by activating GPR120 signaling in myeloid cells.
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