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The GCH1/BH4 pathway acts as an endogenous antioxidant pathway, GCH1 protects cells from ferroptosis primarily through the antioxidant action of BH4, and is completely independent of GPX4-mediated protection against ferroptosis [44]
Skin damage, however, is also a problem
Then, multiple studies have confirmed that Nrf2 can regulate a host of genes associated with ferroptosis, such as ferroportin (FPN), GPX4, small heterodimer partner (SHP) and peroxisome proliferator-activated receptor (PPAR)[50, 128]
In this context, the low level of GSTFU20 transcripts may be accompanied by a high extent of translational efficiency, leading to an increase in protein abundance
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