We explored how eicosapentaenoic acid (EPA) and its metabolites can protect heart cells during a heart attack, specifically focusing on a laboratory model for ischemic injury. Our investigation centered on a specific receptor found in heart cells, known as the Free Fatty Acid Receptor 4 (Ffar4).
In our experiments, cardiac myocytes, or heart cells, were exposed to a controlled environment mimicking conditions of reduced blood flow followed by reoxygenation, essentially simulating a heart attack scenario. Applying an Ffar4 agonist, TUG-891, along with EPA-derived components like 18-hydroxyeicosapentaenoic acid (18-HEPE) and resolvin E1 (RvE1), we observed a significant reduction in harmful reactive oxygen species and heart cell death.
Notably, blocking the ChemR23 receptor with a specific antagonist negated the protective effects we noted from these treatments. This finding highlights that Ffar4 and ChemR23 work together in heart cells to defend against the damage that occurs after ischemic injury.
Overall, our data reinforce the idea that eicosapentaenoic acid has beneficial roles in protecting heart cells from ischemia, meriting further exploration as a potential therapeutic in heart attack management.