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However, the pathological mechanisms underlying cerebral ischemia reperfusion injury (CIRI) after CPR are very complex and involve calcium overload, mitochondrial dysfunction, inflammatory responses, apoptosis, the accumulation of oxygen free radicals, and the excessive release of excitatory amino acids[19]

Although FOXO4s specific effects on mitochondria are as direct as the other peptides above, it is known to regulate the expression of genes involved in oxidative stress response and energy metabolism, which can impact mitochondrial function indirectly (Liu, 2019)

This underlines the intricate involvement of CER in the regulation of iron-related cellular processes and its role in mitigating ferroptosis responses in HCC cells

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