幽门螺杆菌感染引起胃黏膜解痉多肽表达化生机制
Mechanism of spasmolytic polypeptide-expressing metaplasia in gastric mucosa induced by Helicobacter pylori infection
王海诺 1李玙璠 1王雨莹 1沈倩影 2朱进霞 2郑丽飞2
作者信息
- 1. 首都医科大学 基础医学院,北京 100069
- 2. 首都医科大学 基础医学院 生理学与病理生理学系,北京 100069
- 折叠
摘要
幽门螺杆菌(H.pylori)感染后胃黏膜会发生炎性反应和解痉多肽表达化生(SPEM).这些病症会进一步诱导慢性胃炎、胃溃疡,甚至胃癌.因此,SPEM通常被认为是胃黏膜损伤和癌变的早期指标之一.阐明H.pylori诱导的SPEM细胞来源和分子调控可以更深入地了解相关胃黏膜疾病的发病机制,并为其疾病的诊断和治疗提供新的思路和靶点.本文对SPEM相关的分子标志物进行了总结,阐述了TFF2、CD44v9 和AQP5 在H.pylori感染和SPEM中的调控作用.对SPEM细胞的起源以及相关分子调控机制进行了综述.
Abstract
Helicobacter pylori(H.pylori)infection triggers gastric mucosal inflammatory responses and spasmolytic polypeptide-expressing metaplasia(SPEM).These pathological conditions can escalate the severity of chronic gas-tritis,gastric ulcers and even cause gastric cancer.SPEM is frequently viewed as an early sign of gastric mucosal injury and the onset of carcinogenesis.A comprehensive analysis of the genesis and molecular regulation of SPEM cells in the context of H.pylori infection further has enlightened the pathogenesis of gastric mucosal diseases and provide new ideas and targets for diagnosing and treatment of H.pylori-related gastric mucosal diseases.This paper reviews a variety of molecular biomarkers associated with SPEM,encompassing TFF2,CD44v9,and AQP5,and delineates their pivotal regulatory functions in H.pylori infection and SPEM.This paper also reviews the origination of SPEM cells and pertinent molecular regulatory mechanisms.
关键词
幽门螺杆菌/胃黏膜解痉多肽表达化生Key words
Helicobacter pylori/spasmolytic polypeptide-expressing metaplasia引用本文复制引用
出版年
2025
国家科技期刊平台
NSTL
万方数据