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Lipotoxicity (i.e., damage caused by the inappropriate accumulation of lipids in non-adipose tissue), inflammation, and oxidative stress have all been shown to contribute to obesity-associated ER stress (Fu, Watkins, & Hotamisligil, 2012

pylori infection enhances the proliferation and migration of gastric epithelial cells

However, HP possesses a self-protection mechanism, which not only neutralizes the damage caused by gastric acid through ammonia but also simulates the proton channel by Urel protein to suppress the release of gastric acid during colonization

From biomolecular aspects to possible therapeutic interventions