首页|幽门螺杆菌相关细胞凋亡在胃癌发生中的作用机制研究进展

幽门螺杆菌相关细胞凋亡在胃癌发生中的作用机制研究进展

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目的 了解与幽门螺杆菌(Helicobacter pylori,H.pylori)相关的细胞凋亡在胃癌发生中的作用机制,探讨细胞凋亡与胃癌之间的关系.方法 检索近年来国内外关于与H.pylori相关的细胞凋亡在胃癌中作用机制相关研究的文献并进行综述.结果 H.pylori感染是胃癌发生和发展过程中的重要危险因素之一,胃上皮细胞和胃微环境中的多种细胞成分相互作用的平衡失调是其感染特征,这些机制通常促进或抑制细胞凋亡过程,进而干预胃癌进程.结论 H.pylori通过调节多种细胞成分和分子通路增强了胃黏膜上皮细胞对细胞凋亡的敏感性,从而参与胃癌进程;随着精准医学时代的到来,与H.pylori相关的细胞凋亡在胃癌中的机制研究向临床发生转化,有望为胃癌患者提供新的治疗策略.
Progress of Helicobacter pylori-related cell apoptosis in mechanisms of gastric carcinogenesis
Objective To understand the mechanisms of gastric carcinogenesis relevant to Helicobacter pylori(H.pylori)-related cell apoptosis and explore potential causes of gastric cancer development through cell apoptosis.Method The literature of recently domestic and international research on the mechanisms of H.pylori-related cell apoptosis in the gastric carcinogenesis was searched and reviewed.Results The H.pylori infection was one of the important risk factors in the occurrence and development of gastric cancer,which was characterized by the imbalance of the interaction between gastric epithelial cells and various cell components in the gastric microenvironment,and which promoted or inhibited the process of apoptosis,and thus interfered with the process of gastric cancer.Conclusions H.pylori,through the regulation of various cellular components and molecular pathways,increases the sensitivity of gastric epithelial cells to apoptosis,actively participates in the progression of gastric cancer.With the advent of the era of precision medicine,research on the mechanisms of H.pylori-related cell apoptosis in gastric carcinogenesis is transitioning to clinical applications,offering promising new treatment strategies for gastric cancer patients.

gastric cancerHelicobacter pyloricell apoptosis

吴紫瑶、马继春、李兴亮、潘志昂、朱次巴、达明绪

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兰州大学第一临床医学院(兰州 730000)

兰州大学(兰州 730000)

甘肃省人民医院肿瘤外科(兰州 730000)

甘肃中医药大学第一临床医学院(兰州 730000)

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胃癌 幽门螺杆菌 细胞凋亡

国家自然科学基金资助项目甘肃省科技计划项目-自然科学基金

8216058822JR11RA252

2024

中国普外基础与临床杂志
四川大学华西医院

中国普外基础与临床杂志

CSTPCD
影响因子:0.858
ISSN:1007-9424
年,卷(期):2024.31(1)
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