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. 2022 Sep 23;9:1003340. doi: 10.3389/fnut.2022.1003340

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Copyright © 2022 Zhang, Liu, Dai, Wang, Wu, Su and Zhang.

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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Vitamins and regulated necrosis. (A) Vitamin E. Vitamin E (VitE) attenuates regulated necrosis through downregulating the intracellular ROS. As lipophilic antioxidants, VitE can directly remove the lipid peroxides that accumulate in the cell. Meanwhile, VitE inhibits the activity of LOXs, which also blocks the lipid peroxidation. (B) Vitamin D. Vitamin D (VitD) activates vitamin D receptor (VDR), which (i) inhibits the formation of necrosome to block necroptosis; (ii) upregulates the expression of GPX4 to inhibit lipid peroxidation and resultant ferroptosis; (iii) inactivates inflammasome directly or via autophagy to inhibit pyroptosis. (C) Vitamin C. Vitamin C (VitC) upregulates the expression of RIPK1, RIPK3, and MLKL, which triggers necroptosis. In addition, VitC triggers lipid peroxidation by (i) inactivating GPX4: (ii) increasing the intracellular ferrous iron. The accumulated lipid peroxides lead to ferroptosis.