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This variability likely stems from tissue-specific differences in iron demand, metabolic activity, regulation, and susceptibility to iron-induced cellular damage that requires further clarification

Multiple roles of peroxiredoxins in inflammation

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FTL and FTH1, the light and heavy chains of FT, are regulated by Nrf2

This phenomenon can be abrogated by tempolan ROS scavengerthe antioxidant N-acetylcysteine, or NF-B inhibitors, but not the AhR blocker, which means that IS-induced hepcidin production occurs as a result of oxidative-stress-activated NF-B signaling, and is independent of the AhR-mediated pathway [124]