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For the in vitro experiments, silencing CA9 abrogated ATT-I-mediated Claudin-1, Occludin, GPX4 and SLC7A11 upregulation in Erastin-treated Caco-2 cells, indicating that CA9 is an indispensable mediator for ATT-I to restrain Erastin-induced ferroptosis in Caco-2 cells

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With aging, cumulative alterations occur across all layers of this multilayered structure, resulting in impaired barrier integrity, diminished regenerative capacity, and increased susceptibility to environmental insults [33]

& Pagano, M

The extent of this phenomenon is poorly documented in the scientific litterature