Fig. 13

Helicobacter infects and survives in the stomach via various pathogenic factors. Helicobacter causes damage to the host and ultimately causes tumors via oxidative stress, inflammation, DNA damage, apoptosis, and proliferation ways. The order in which mechanisms are listed in the figure does not represent their order of occurrence in diseases. HopQ, Hop family adhesin HopQ; cagPAI, cytotoxin-associated gene pathogenicity island; T4SS, type IV secretion system; CagA, cytotoxin-associated gene A protein; HBP, heptose-1, 7-bisphosphate; T5SS, type V secretion system; VacA, vacuolating cytotoxin A; iNOS, isoform of nitric oxide synthase; COX-2, cyclooxygenase-2; MPO, myeloperoxidase; IL, interleukin; IFN-γ, interferon-gamma; TNF-α, tumor necrosis factor-α; TGF-β, transforming growth factor-β; Bax, Bcl-2-associated X protein; Bad, Bcl-2-associated agonist of cell death; Apaf-1, apoptotic protease activating factor-1; Bcl-2, B-cell lymphoma-2 protein; Bcl-xl, Bcl-2-like protein-1; ROS, reactive oxygen species; LPO, lipid peroxide; MDA, malondialdehyde; LDH, lactatedehydrogenase; Keap1, kelch-like ECH-associated protein 1; NRF2, nuclear factor erythroid-2-related factor 2; HO-1, heme oxygenase-1; pH2AX, phospho-histone H2A. X; 8-OHdG, 8-hydroxydeoxyguanosine; Mcl-1, myeloid cell leukemia protein 1; EGFR, epidermal growth factor receptor; ADAM, a disintegrin and metalloproteinase; BrdU, 5’-bromodeoxyuridine; Ki-67, antigen identified by monoclonal antibody Ki-67.