ArticleScientific reports2024
Helicobacter pylori CagA mediated mitophagy to attenuate the NLRP3 inflammasome activation and enhance the survival of infected cells.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Mitophagy interacts with mitochondrial dynamics and biogenesis, acting as a double-edged sword in digestive cancer.iScience · 2026Review
- The Oral-Gastric Microbial Axis in Gastric Cancer: Mechanisms Underlying Development and Progression.Cancers · 2026Review
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- Pathological effects of diabetic mice withWorld journal of diabetes · 2026Article
- Increasing autophagy activity suppressesAmerican journal of cancer research · 2026Article
- Mitochondria-lysosome crosstalk in microbial infections.Science China. Life sciences · 2025Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Biphasic Adaptations of Gastric Epithelial Cells in ChronicInternational journal of molecular sciences · 2025Article
- Are an Aging Gut and a Decrease in Butyrate Production the Reasons for Atherosclerosis?International journal of molecular sciences · 2025Review
- Jatrorrhizine attenuates inflammatory response in Helicobacter pylori-induced gastritis by suppressing NLRP3 inflammasomes and NF-κB signaling pathway.Archives of microbiology · 2025Article
- Article
- Influence of helicobacter pylori infection on Chinese adult males' body muscle mass: a cross-sectional and cohort analysis.Frontiers in cellular and infection microbiology · 2025Article
- Microbiome influence in gastric cancer progression and therapeutic strategies.Frontiers in medicine · 2025Review
- Genomic epidemiology ofFrontiers in microbiology · 2025Article
- Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024Review
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Authors and funding
11 authors.
Funding
Abstract
Helicobacter pylori (H. pylori) is one of the most common bacterial infections in the world, and its key virulence component CagA is the leading cause of gastric cancer. Mitophagy is a form of selective autophagy that eliminates damaged mitochondria and is essential for some viruses and bacteria to evade the immune system. However, the mechanisms by which CagA mediates H. pylori-induced mitophagy and NLRP3 inflammasome activation remain elusive. In this study, we reported that H. pylori primarily uses its CagA to induce mitochondrial oxidative damage, mitochondrial dysfunction, dynamic imbalance, and to block autophagic flux. Inhibition of mitophagy led to an increase in NLRP3 inflammasome activation and apoptosis and a decrease in the viability of H. pylori-infected cells. Our findings suggested that H. pylori induces mitochondrial dysfunction and mitophagy primarily via CagA. It reduces NLRP3 inflammasome activation to evade host immune surveillance and increases the survival and viability of infected cells, potentially leading to gastric cancer initiation and development. Our findings provide new insights into the pathogenesis of H. pylori-induced gastric cancer, and inhibition of mitophagy may be one of the novel techniques for the prevention and treatment of this disease.
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