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In the liver study, however, compounds that remain after decaffeination appear to be an important part of the explanation
Nrf2 upregulates the expression of dozens of cytoprotective enzymes, including GCL itself, creating a compensatory response to oxidative stress
Extending these findings to mammalian nerve repair, we show that loss of Glutathione peroxidase 4 (GPX4), a crucial suppressor of ferroptosis, promotes functional recovery after sciatic nerve injury
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