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In the IL-10-deficient mouse model, depletion of mucin and a reduction in Akkermansia bacteria occurred prior to the onset of inflammation, suggesting that barrier dysfunction may be a triggering factor for IBD [74]

ROS are generated within the inner mitochondrial membrane as byproducts of oxidative phosphorylation (OXPHOS), making mitochondria a major source of intracellular ROS [37, 38]

albicans can transform from a symbiotic state to a pathogenic state, which may occur under conditions of host immune dysfunction, dysbiosis of the colonizing microbiota, or damage to the intestinal mucosal barrier (Zhai et al., 2020)

As a result, intracellular Fe2+ accumulates, ROS levels increase, and cellular sensitivity to ferroptosis is enhanced

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