He Qijin, Liu Limin, Wei Jingge, Jiang Jiaying, Rong Zheng, Chen Xin, Zhao Jingwen, Jiang Kui
Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, No. 154 Anshan Road, Tianjin, 300052, China.
Cell Death Discov. 2022 Apr 4;8(1):158. doi: 10.1038/s41420-022-00962-1.
Gastric intestinal metaplasia (IM) is a precancerous lesion that increases the risk of subsequent gastric cancer (GC) development. Therefore, the mechanism of IM has been the focus of basic and clinical research. Helicobacter pylori (H. pylori) infection has been recognized as the main pathogenesis of gastric IM. However, more and more studies have shown that chronic inflammation of gastric mucosa caused by bile reflux is the key pathogenic factor of gastric IM. Bile reflux activates the expression of IM biomarkers via the bile acid receptor. In addition, microRNAs, exosomes, and epigenetics are also involved in the occurrence and development of bile acid-induced gastric IM. Currently, the relevant research is still very few. The molecular mechanism of the phenotypic transformation of gastrointestinal epithelial cells induced by bile acids has not been fully understood. This article mainly reviews the physiology and pathology of bile acid, mechanism of gastric IM induced by bile acid, bile acid receptors, and so on, in order to provide reference for further research.
胃黏膜肠化生（IM）是一种癌前病变，会增加后续发生胃癌（GC）的风险。因此，IM的发病机制一直是基础和临床研究的重点。幽门螺杆菌（H. pylori）感染已被公认为胃IM的主要发病机制。然而，越来越多的研究表明，胆汁反流引起的胃黏膜慢性炎症是胃IM的关键致病因素。胆汁反流通过胆汁酸受体激活IM生物标志物的表达。此外，微小RNA、外泌体和表观遗传学也参与了胆汁酸诱导的胃IM的发生和发展。目前，相关研究仍然很少。胆汁酸诱导胃肠道上皮细胞表型转化的分子机制尚未完全明确。本文主要综述胆汁酸的生理和病理、胆汁酸诱导胃IM的机制、胆汁酸受体等，以期为进一步研究提供参考。
