期刊
REDOX REPORT
卷 16, 期 1, 页码 1-7出版社
TAYLOR & FRANCIS LTD
DOI: 10.1179/174329211X12968219310756
关键词
Carcinogenesis; Gastric epithelial cells; Helicobacter pylori; Inflammatory cells
资金
- Japan Society for the Promotion of Science [21390184, 22590705]
- City Area Program
- Ministry of Education, Culture, Sports, Science and Technology, Japan
- Adaptable and Seamless Technology Transfer Program through target-driven RD
- Japan Science and Technology Agency
Almost half the world's population is infected by Helicobacter pylori (H. pylori). This bacterium increases the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in human stomach, and this has been reported to impact upon gastric inflammation and carcinogenesis. However, the precise mechanism by which H. pylori induces gastric carcinogenesis is presently unclear. Although the main source of ROS/RNS production is possibly the host neutrophil, H. pylori itself produces O-2(center dot-). Furthermore, its cytotoxin induces ROS production by gastric epithelial cells, which might affect intracellular signal transduction, resulting in gastric carcinogenesis. Excessive ROS production in gastric epithelial cells can cause DNA damage and thus might be involved in gastric carcinogenesis. Understanding the molecular mechanism of H. pylori-induced carcinogenesis is important for developing new strategies against gastric cancer.
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