Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review

Abstract

Chronic atrophic gastritis (CAG) is a prevalent digestive system disease characterized by atrophy of the gastric mucosa and the disappearance of inherent gastric glands. According to the theory of Correa's cascade, CAG is an important pathological stage in the transformation from normal condition to gastric carcinoma. In recent years, the global incidence of CAG has been increasing due to pathogenic factors, including Helicobacter pylori infection, bile reflux, and the consumption of processed meats. In this review, we comprehensively described the etiology and clinical diagnosis of CAG. We focused on elucidating the regulatory mechanisms and promising therapeutic targets in CAG, with the expectation of providing insights and theoretical support for future research on CAG.

Keywords: biomarkers; chronic atrophic gastritis; gastric precancerous lesions; pathogenetic mechanisms; therapeutic targets.

FIGURE 1

The symptoms, etiology, and clinical diagnosis of CAG.

FIGURE 2

Programmed cell death in CAG. Programmed cell death is involved in the pathogenesis of CAG, including apoptosis, autophagy, pyroptosis, and ferroptosis. HP, acting as an avital pathogenic factor, can regulate programmed cell death and affect the development of CAG.

FIGURE 3

Signaling pathways and targets regulating CAG development. The development of CAG is achieved by numerous signaling pathways and targets, including NF-κB pathway, Hedgehog pathway, TLRs pathway, PI3K/Akt pathway, MAPK pathway, Wnt/β-catenin pathway, p53 pathway, and Hippo pathway.

FIGURE 4

Novel mechanisms regulating CAG development. Recent studies have found that other novel mechanisms are associated with the regulation of CAG development, including angiogenesis, energy metabolism, gut microbiota and gastric microbiota, inflammatory microenvironment, oxidative stress, gastric stem cells defect, non-coding RNAs, and exosomes.