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The compromised barrier allows for the translocation of luminal microbial components, which, along with damage signals from dying cells, activates inflammatory pathways This triggers a positive feedback loop involving oxidative stress, lipid peroxidation, the release of pro-inflammatory cytokines, and the activation of matrix-degrading enzymes with concomitant downregulation of junction proteins that permit microbial invasion

Abnormally elevated lipid ROS levels are regulated by GPX4, 91 which can effectively repair the oxidative damage of mammalian unsaturated fatty acids and thus inhibit the occurrence of ferroptosis