TY - JOUR
T1 - Research on drug treatment and the novel signaling pathway of chronic atrophic gastritis
AU - Jao, Jinhao
AU - Zhao, Huijie
AU - Li, Fangfei
AU - Zheng, Qinsheung
AU - Wang, Guoli
AU - Li, Defang
AU - Liu, Ying
N1 - This research was funded by the National Natural Science Foundation of China (82073313 to D.L.), the joint project of State Administration of Traditional Chinese Medicine and Health Commission of Shandong Provincial (GZY-KJS-SD-2023–094), the Traditional Chinese Medicine Special Project of Binzhou Medical University Affiliated Traditional Chinese Medicine Hospital (2023ZYZX02), 2023 Qilu Biancang Traditional Chinese Medicine Talent Cultivation Project (to D. L.), and the Introduction and Cultivation Project for Young Creative Talents of Higher Education of Shandong Province (to G.W).
PY - 2024/7
Y1 - 2024/7
N2 - 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.
AB - 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.
KW - Chronic atrophic gastritis
KW - Helicobacter pylori
KW - MAPK
KW - NF-κB
KW - PI3K/AKT
KW - Wnt/β-catenin
UR - https://www.sciencedirect.com/science/article/pii/S0753332224007960
UR - http://www.scopus.com/inward/record.url?scp=85195164741&partnerID=8YFLogxK
U2 - 10.1016/j.biopha.2024.116912
DO - 10.1016/j.biopha.2024.116912
M3 - Journal article
SN - 0753-3322
VL - 176
JO - Biomedicine and Pharmacotherapy
JF - Biomedicine and Pharmacotherapy
M1 - 116912
ER -