Helicobacter pylori and Gastric Cancer: Adaptive Cellular Mechanisms Involved in Disease Progression.
Helicobacter pylori and Gastric Cancer: Adaptive Cellular Mechanisms Involved in Disease Progression.
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幽门螺杆菌和胃癌：参与疾病进展的适应性细胞机制。
DOI：
10.3389/fmicb.2018.00005
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发表时间：
2018
影响因子：
5.2
通讯作者：
Quest AFG
中科院分区：
文献类型：
--
作者：
Díaz P;Valenzuela Valderrama M;Bravo J;Quest AFG
幽门螺杆菌（H.幽门螺杆菌感染是导致胃癌的主要危险因素。从正常粘膜到非萎缩性胃炎的转变，主要由H。幽门螺杆菌感染，启动癌前病变，然后可能进展为萎缩性胃炎和肠上皮化生。一般认为，进一步发展为异型增生和胃癌是由于不再需要H的存在的过程。幽门。对H.幽门螺杆菌感染是通过细菌毒力因子的作用直接介导的，这些毒力因子驱动与受感染胃细胞转化相关的初始事件。除了遗传和迄今为止定义不清的环境因素外，H。幽门螺杆菌似乎是至关重要的慢性感染和胃病的进展。首先，H.幽门螺杆菌感染促进胃细胞死亡，并减少大多数感染细胞的上皮细胞更新，导致与初始炎症反应相关的原发性组织损伤。然而，在剩余的胃细胞群中，诱导适应性反应，增加细胞存活和增殖，导致获得可能导致胃癌前病变的潜在恶性特征。因此，这些内在的生存相关反应的失调H。幽门螺杆菌感染是促进疾病进展的潜在罪魁祸首。本文将重点介绍H.幽门螺杆菌感染，包括内质网应激和未折叠蛋白反应，自噬，氧化应激和炎症，以及随后的讨论如何这些因素可能参与癌前病变的进展。最后，这篇综述将阐明这些机制如何被利用作为药理学靶点，在胃癌的非侵入性风险控制开辟新的治疗选择的角度。
Helicobacter pylori (H. pylori) infection is the major risk factor associated with the development of gastric cancer. The transition from normal mucosa to non-atrophic gastritis, triggered primarily by H. pylori infection, initiates precancerous lesions which may then progress to atrophic gastritis and intestinal metaplasia. Further progression to dysplasia and gastric cancer is generally believed to be attributable to processes that no longer require the presence of H. pylori. The responses that develop upon H. pylori infection are directly mediated through the action of bacterial virulence factors, which drive the initial events associated with transformation of infected gastric cells. Besides genetic and to date poorly defined environmental factors, alterations in gastric cell stress-adaptive mechanisms due to H. pylori appear to be crucial during chronic infection and gastric disease progression. Firstly, H. pylori infection promotes gastric cell death and reduced epithelial cell turnover in the majority of infected cells, resulting in primary tissue lesions associated with an initial inflammatory response. However, in the remaining gastric cell population, adaptive responses are induced that increase cell survival and proliferation, resulting in the acquisition of potentially malignant characteristics that may lead to precancerous gastric lesions. Thus, deregulation of these intrinsic survival-related responses to H. pylori infection emerge as potential culprits in promoting disease progression. This review will highlight the most relevant cellular adaptive mechanisms triggered upon H. pylori infection, including endoplasmic reticulum stress and the unfolded protein response, autophagy, oxidative stress, and inflammation, together with a subsequent discussion on how these factors may participate in the progression of a precancerous lesion. Finally, this review will shed light on how these mechanisms may be exploited as pharmacological targets, in the perspective of opening up new therapeutic alternatives for non-invasive risk control in gastric cancer.
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影响因子：
11.1
作者：
He C;Klionsky DJ
通讯作者：
Klionsky DJ
影响因子：
7.4
作者：
Chen, Hai-Ning;Wang, Zhu;Zhou, Zong-Guang
通讯作者：
Zhou, Zong-Guang
影响因子：
3.1
作者：
Ding, Song-Ze;Minohara, Yutaka;Crowe, Sheila E.
通讯作者：
Crowe, Sheila E.
DOI：
10.1016/j.biocel.2010.04.015
发表时间：
2010-09-01
影响因子：
4
作者：
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通讯作者：
Kim, Hyeyong
影响因子：
29.4
作者：
Gong, Min;Ling, Samantha Shi Min;Ho, Bow
通讯作者：
Ho, Bow