Research on drug treatment and the novel signaling pathway of chronic atrophic gastritis

• Published in: Biomedicine & pharmacotherapy Vol. 176; p. 116912
• Main Authors: Jia, Jinhao, Zhao, Huijie, Li, Fangfei, Zheng, Qiusheng, Wang, Guoli, Li, Defang, Liu, Ying
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.07.2024; Elsevier
• Subjects: Chronic atrophic gastritis; Helicobacter pylori; MAPK; NF-κB; PI3K/AKT; Wnt/β-catenin; NF-κB; Helicobacter pylori; MAPK; Wnt/β-catenin; Chronic atrophic gastritis; PI3K/AKT
• ISSN: 0753-3322; 1950-6007; 1950-6007
• DOI: 10.1016/j.biopha.2024.116912

Chronic atrophic gastritis (CAG) is a global digestive system disease and one of the important causes of gastric cancer. The incidence of CAG has been increasing yearly worldwide. This article reviews the latest research on the common causes and future therapeutic targets of CAG as well as the pharmacological effects of corresponding clinical drugs. We provide a detailed theoretical basis for further research on possible methods for the treatment of CAG and reversal of the CAG process. CAG often develops from chronic gastritis, and its main pathological manifestation is atrophy of the gastric mucosa, which can develop into gastric cancer. The drug treatment of CAG can be divided into agents that regulate gastric acid secretion, eradicate Helicobacter. pylori (H. pylori), protect gastric mucous membrane, or inhibit inflammatory factors according to their mechanism of action. Although there are limited specific drugs for the treatment of CAG, progress is being made in defining the pathogenesis and therapeutic targets of the disease. Growing evidence shows that NF-κB, PI3K/AKT, Wnt/ β-catenin, MAPK, Toll-like receptors (TLRs), Hedgehog, and VEGF signaling pathways play an important role in the development of CAG. [Display omitted] •Chronic atrophic gastritis (CAG) is one of the commonest digestive diseases worldwide.•Drugs for CAG include proton pump inhibitors, H2 receptor antagonists, gastric mucosal protectants, and others.•NF-κB, PI3K/AKT, Wnt/β-catenin, MAPK, TLRs, Hedgehog and VEGF signaling pathways play an important role in CAG.