【摘要】 幽门螺杆菌(Helicobacter pylori,H.pylori)感染作为全球重大公共卫生问题，与慢性胃炎、消化性溃疡及胃癌等多种胃部疾病密切相关。H.pylori通过直接毒力因子作用及宿主免疫调控介导胃黏膜损伤，其致病机制涉及TLRs通路、NLRP3炎症小体通路、NF-κB通路、MAPK通路、JAK/STAT与PI3K/AKT通路。此外，H.pylori通过调控自噬稳态失衡、凋亡逃逸及表观遗传重塑维持慢性感染并促进癌前病变。本文就H.pylori感染诱发胃黏膜损伤涉及的关键信号通路及分子机制作一概述。更多还原

【Abstract】 Helicobacter pylori(H.pylori) infection, a major global public health concern, is closely associated with various gastric diseases, including chronic gastritis, peptic ulcers, and gastric cancer. H.pylori mediates gastric mucosal injury through direct virulence factor activity and host immune regulation. Its pathogenic mechanisms involve multiple signaling pathways, such as the TLRs pathway, NLRP3 inflammasome pathway, NF-κB pathway, MAPK pathway, JAK/STAT and PI3K/AKT pathways. Additionally, H.pylori sustains chronic infection and promotes precancerous lesions by regulating autophagy dysregulation, apoptotic evasion, and epigenetic remodeling. This article summarized the key signaling pathways and molecular mechanisms underlying H.pylori-induced gastric mucosal injury.更多还原