Helicobacter pylori (Hp) is classified as a group Ⅰ carcinogen and serves as a major pathogenic factor in the development of gastric cancer. Studies have confirmed that eradicating Hp can reduce gastric cancer mortality. Although standard therapies combining proton pump inhibitors with antibiotics have shown some efficacy, increasing drug resistance and adverse effects have led to a continuous decline in the eradication rate of Hp. Therefore, there is an urgent need to develop novel therapeutic strategies to improve the cure rate of Hp infection. This article focuses on the mechanisms by which Hp induces mitochondrial dysfunction, including mediating mitochondrial oxidative stress, alterations in mitochondrial dynamics, mitochondrial autophagy (mitophagy), and mtDNA damage. By delving into the pathogenesis of Hp-related diseases triggered by mitochondrial dysfunction, this review aims to provide a theoretical foundation for identifying new clinical targets for the prevention and treatment of Hp infection.