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

Jinhao Jao, Huijie Zhao, Fangfei Li, Qinsheung Zheng, Guoli Wang, Defang Li*, Ying Liu*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review


Background: 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. Purpose: 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. Results: 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.
Original languageEnglish
Article number116912
Number of pages20
JournalBiomedicine and Pharmacotherapy
Early online date7 Jun 2024
Publication statusPublished - Jul 2024

Scopus Subject Areas

  • Pharmacology

User-Defined Keywords

  • Chronic atrophic gastritis
  • Helicobacter pylori
  • MAPK
  • NF-κB
  • PI3K/AKT
  • Wnt/β-catenin


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