幽门螺杆菌与H⁺-K⁺-ATP酶在胃癌发病中的研究进展

Research Advances of Helicobacter pylori and H⁺-K⁺-ATPase in the Pathogenesis of Gastric Cancer

胃癌是上消化道最常见的恶性肿瘤之一,幽门螺杆菌(Helicobacter pylori, H. pylori)感染是其发病的主要危险因素,但是,幽门螺杆菌在胃癌发生过程中的具体机制仍未阐明。H+-K+-ATP酶在胃粘膜壁细胞保持正常结构、维持正常的胃内酸性环境中起着重要作用,当H+-K+-ATP酶表达过低会导致胃酸分泌减少,使胃粘膜发生萎缩,最终进展为癌症。幽门螺杆菌感染后可以改变H+-K+-ATP酶的表达,共同参与胃癌的发生发展。因此,本文对幽门螺杆菌感染与H+-K+-ATP酶在胃癌在胃癌发病机制中的作用作一综述。

Gastric cancer is one of the most common malignant tumors in the upper digestive tract, and Heli-cobacter pylori (H. pylori) infection is the main risk factor. However, the specific mechanism of Heli-cobacter pylori in the development of gastric cancer remains unclear. H+-K+-ATPase plays an im-portant role in maintaining the normal structure of gastric mucosal parietal cells and maintaining the normal gastric acidic environment. When H+-K+-ATPase expression is too low, the gastric acid secretion will be reduced, and the gastric mucosa will atrophy and eventually progress to cancer. Helicobacter pylori infection can change the expression of H+-K+-ATPase and participate in the oc-currence and development of gastric cancer. Therefore, this paper reviews the role of Helicobacter pylori infection and H+-K+-ATPase in the pathogenesis of gastric cancer.