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. 2024 Jul 31;14:1416819. doi: 10.3389/fcimb.2024.1416819

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Copyright © 2024 Lin, Liu, Lu, Zhai and Cheng

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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Apoptosis in chronic H. pylori infection. In chronic infection, H. pylori can trigger dysregulation of the BCL-2 system and downregulate apoptosis. H. pylori also leads to chronic inflammation, triggers oxidative stress and inhibits apoptosis. CagA, the virulence factor released by H. pylori, can regulate the activation of PI3K and AKT. AKT-dependent phosphorylation of caspase-9 attenuates apoptosis. All these dysregulations of apoptosis in chronic infection lead to the formation of a tumor microenvironment and ultimately contribute to the development of gastric cancer.