Figure 6.

EPA’s role in reducing oxidative stress within cardiomyocytes. Under normal conditions, EPA (eicosapentaenoic acid) is involved in various cellular processes that promote mitochondrial efficiency and protect against dysfunction. During conditions of oxidative stress, EPA is shown to reduce the breakdown of cardiolipin and mitigate mitochondrial dysfunction. It improves O2 consumption efficiency by Complex IV in the mitochondrial membrane, facilitated by MnSOD (manganese superoxide dismutase). EPA also prevents the translocation of Fyn to the cell membrane, thereby inhibiting the activation of Rho Kinase. Additionally, EPA interacts with Ffar4, leading to the production of 18-HEPE. EPA also activates transcription factor Nrf2. This interaction results in altered gene expression through Nrf2 and 18-HEPE, which enhances the expression of antioxidant enzymes, including heme-oxygenase-1.