萎缩性胃炎
幽门螺杆菌
衰老
端粒
自噬
细胞衰老
癌症
生物
病态的
炎症
胃炎
DNA甲基化
免疫学
癌症研究
医学
病理
表型
基因
遗传学
细胞凋亡
基因表达
作者
Shi‐yu Zheng,Lu Zhu,Luyi Wu,Hui‐rong Liu,Xiao‐peng Ma,Qi Li,Meng‐die Wu,W Wang,Jing Li,Huangan Wu
摘要
Background Chronic atrophic gastritis (CAG) is a pathological stage in the Correa's cascade, whereby Helicobacter pylori (H. pylori) infection is the primary cause. Cellular senescence is an inducing factor for cancer occurrence and cellular senescence is an obvious phenomenon in gastric mucosal tissues of H. pylori-positive CAG patients. Methods In this review, we collated the information on cellular senescence and H. pylori-positive CAG. Results At present, only a few studies have observed the effect of cellular senescence on precancerous lesions. In combination with the latest research, this review has collated the information on cellular senescence and H. pylori-positive CAG from four aspects- telomere shortening, DNA methylation, increased reacive oxygen species (ROS) production, and failure of autophagy. Conclusion This is expected to be helpful for exploring the relevant mechanisms underlying inflammatory cancerous transformation and formulating appropriate treatment strategies.
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