Altered expression of ferroptosis markers and iron metabolism reveals a potential role of ferroptosis in vitiligo

Oxidative stress is one of the triggering factors for vitiligo, which leads to melanocyte (MC) destruction in vitiligo lesions. Ferroptosis, which is characterized by iron-dependent increase in oxidative stress and lipid peroxidation, has been widely explored in numerous diseases, whereas whether ferroptosis plays a role in MC loss of vitiligo remains to be elucidated. Quantitative real-time PCR and western blot analysis were used to determine the expression of ferroptosis markers in vitiligo patients. Immunonephelometry and electrochemiluminescence were performed to analyze iron status. Reactive oxygen species (ROS), Fe2+, and lipid ROS were assessed by flow cytometry. The expression of ferroptosis markers was significantly altered in the epidermis of vitiligo patients. Iron deficiency was revealed in the blood of patients. Erastin reduced cell viability and led to oxidative stress, iron overload as well as lipid peroxide accumulation in human epidermal MCs in vitro. Altered expression of ferroptosis markers and inhibition of melanin synthesis in MCs were induced by erastin, which was attenuated by N-acetyl-L-cysteine (NAC) pretreatment or post-treatment in vitro. In conclusion, ferroptosis might take place during the process of vitiligo. Erastin could induce ferroptosis in human epidermal MCs and NAC could protect MCs from ferroptosis in vitro.

Automated summary

The expression of ferroptosis markers is altered in the epidermis of vitiligo patients and iron deficiency is revealed in their blood. Erastin induces ferroptosis in human epidermal MCs in vitro, while NAC protects MCs from ferroptosis.