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10.1016/j.amjcard.2018.11.02730527777 151 Yang B, Ma K, Xiang R, et al

The overexpression and knockdown of GPX4 can modulate the lethality of various ferroptosis inducers, suggesting that GPX4 is a key regulatory factor in ferroptosis-induced cancer cell death ( However, when GSH levels decrease or GPX4 activity is inhibited, GBM cells can activate alternative antioxidant pathways to maintain redox homeostasis, among which the ferroptosis suppressor protein 1 (FSP1)/coenzyme Q10 (CoQ10) system is the most representative compensatory mechanism ( 3 Interaction between ferroptosis and the TIME of GBM 3.1 Direct regulation of immune cell activity and function by ferroptosis Recent studies have shown that ferroptosis plays a key regulatory role in the GBM TIME ( Figure 3 )

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There is also insufficient evidence on the effect of HO-1 SNPs on vitiligo susceptibility despite this gene is the main actor involved in protecting human melanocytes against oxidative stress through the NRF2-ARE pathway (Jian et al