Helicobacter pylori-positive chronic atrophic gastritis and cellular senescence

被引：12
|
作者：
Zheng, Shi-yu [1 ]
Zhu, Lu [1 ]
Wu, Lu-yi [1 ]
Liu, Hui-rong [1 ,2 ]
Ma, Xiao-peng [1 ,2 ]
Li, Qi [1 ]
Wu, Meng-die [1 ]
Wang, Wen-jia [1 ]
Li, Jing [1 ]
Wu, Huan-gan [1 ,2 ]
机构：
[1] Shanghai Univ Tradit Chinese Med, Yueyang Hosp Integrated Tradit Chinese & Western M, 110 Ganhe Rd, Shanghai 200437, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Shanghai Res Inst Acupuncture & Meridian, 650 South Wanping Rd, Shanghai 200030, Peoples R China
来源：
HELICOBACTER | 2023年 / 28卷 / 01期
关键词：
cellular senescence; chronic atrophic gastritis; gastric mucosa; Helicobacter pylori; OXIDATIVE STRESS; DNA-DAMAGE; INTESTINAL METAPLASIA; VACUOLATING CYTOTOXIN; TELOMERE LENGTH; CANCER; AUTOPHAGY; METHYLATION; INFECTION; MITOCHONDRIA;
D O I：
10.1111/hel.12944
中图分类号：
R57 [消化系及腹部疾病];
学科分类号：
摘要：
BackgroundChronic 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. MethodsIn this review, we collated the information on cellular senescence and H. pylori-positive CAG. ResultsAt 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. ConclusionThis is expected to be helpful for exploring the relevant mechanisms underlying inflammatory cancerous transformation and formulating appropriate treatment strategies.
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页数：8
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