Progress in research of pathogenic factors and signal transduction pathways in Barrett’s esophagus

Barrett's esophagus (BE) is a significant complication of gastroesophageal reflux disease, carrying a high risk of transformation into adenocarcinoma of the esophagus.Its pathological features are the replacement of the squamous epithelium by columnar epithelium in the esophagus, with some accompanied by intestinal metaplasia.This process is extremely complex, involving a multitude of pathogenic factors and signal transduction pathways.Acid reflux and bile acids are the primary pathogenic factors, which can damage the esophageal mucosa, activate inflammatory and oxidative stress responses, and promote intestinal metaplasia by regulating the expression of genes such as CDX2 and MUC2.Additionally, high-fat diet, gastrin, and alterations in esophageal microbiota are also involved.In terms of molecular mechanisms, abnormal activation of signaling pathways such as BMP-4/Smad, Notch, Hedgehog, Wnt, NF-B, and IL-6/STAT3 plays a critical role in the pathogenesis of BE.This article systematically expounds on the potential pathogenic mechanisms of BE and the signal transduction pathways involved, with an aim to provide new insights for the early prevention and targeted therapy of this condition.