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. 2023 Jan 4;10:1079548. doi: 10.3389/fcell.2022.1079548

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Copyright © 2023 Liu, Lian, Shi, Hao and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mll4-specific deficiency in mouse epidermis leads to abnormal expression of several ferroptosis-related genes in keratinocytes, resulting in reduced ferroptotic cell death and consequently affecting normal epidermal differentiation and disrupting the skin barrier. The pathogenesis of autosomal recessive congenital ichthyosis is associated with multiple ALOX genes, and it is hypothesized that ferroptosis may be involved in the pathogenesis of ichthyosis. Mll4: Histone-lysine N-methyltransferase 2D (KMT2D, MLL4); ALOX: arachidonate lipoxygenase; SLC7A11: Solute Carrier Family 7 Member 11; GPX4: Glutathione peroxidases 4.