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本文引用的文献

1
Association between Helicobacter pylori and Barrett's esophagus: a case-control study.幽门螺杆菌与 Barrett 食管的相关性:病例对照研究。
Am J Gastroenterol. 2014 Mar;109(3):357-68. doi: 10.1038/ajg.2013.443. Epub 2014 Jan 14.
2
Barrett's esophagus in 2012: updates in pathogenesis, treatment, and surveillance.2012年的巴雷特食管:发病机制、治疗及监测的最新进展
Curr Gastroenterol Rep. 2013 May;15(5):322. doi: 10.1007/s11894-013-0322-8.
3
Metabolic syndrome as a risk factor for Barrett esophagus: a population-based case-control study.代谢综合征是巴雷特食管的一个危险因素:一项基于人群的病例对照研究。
Mayo Clin Proc. 2013 Feb;88(2):157-65. doi: 10.1016/j.mayocp.2012.09.017.
4
Sox9 drives columnar differentiation of esophageal squamous epithelium: a possible role in the pathogenesis of Barrett's esophagus.Sox9 驱动食管鳞状上皮的柱状分化:在巴雷特食管发病机制中的可能作用。
Am J Physiol Gastrointest Liver Physiol. 2012 Dec 15;303(12):G1335-46. doi: 10.1152/ajpgi.00291.2012. Epub 2012 Oct 11.
5
A global assessment of the oesophageal adenocarcinoma epidemic.全球食管腺癌流行情况评估。
Gut. 2013 Oct;62(10):1406-14. doi: 10.1136/gutjnl-2012-302412. Epub 2012 Aug 23.
6
The role of nitric oxide in the induction of caudal-type homeobox 2 through epidermal growth factor receptor in the development of Barrett's esophagus.一氧化氮在巴雷特食管发育过程中通过表皮生长因子受体诱导尾型同源盒2的作用。
Scand J Gastroenterol. 2012 Oct;47(10):1148-58. doi: 10.3109/00365521.2012.703232. Epub 2012 Jul 27.
7
Hiatal hernia and the risk of Barrett's esophagus.食管裂孔疝与巴雷特食管的风险。
J Gastroenterol Hepatol. 2013 Mar;28(3):415-31. doi: 10.1111/j.1440-1746.2012.07199.x.
8
Evidence for a functional role of epigenetically regulated midcluster HOXB genes in the development of Barrett esophagus.组蛋白修饰调控的中簇 HOXB 基因在 Barrett 食管发生中的功能作用研究
Proc Natl Acad Sci U S A. 2012 Jun 5;109(23):9077-82. doi: 10.1073/pnas.1116933109. Epub 2012 May 17.
9
Notch signaling pathway and Cdx2 expression in the development of Barrett's esophagus.Notch 信号通路与 Cdx2 在 Barrett 食管发育中的表达。
Lab Invest. 2012 Jun;92(6):896-909. doi: 10.1038/labinvest.2012.56. Epub 2012 Mar 26.
10
Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett-like metaplasia.胆汁酸和炎症激活了巴雷特样化生小鼠模型中的胃贲门干细胞。
Cancer Cell. 2012 Jan 17;21(1):36-51. doi: 10.1016/j.ccr.2011.12.004.

巴雷特食管:历史、定义与病因学

Barrett esophagus: history, definition and etiopathogeny.

作者信息

Gindea C, Birla R, Hoara P, Caragui A, Constantinoiu S

机构信息

"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.

出版信息

J Med Life. 2014;7 Spec No. 3(Spec Iss 3):23-30.

PMID:25870690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4391409/
Abstract

The injury of the esophageal epithelium may be determined by the reflux of the gastric acid in the esophagus. Barrett's esophagus (BE) is characterized by the replacement of the normal squamous epithelium with the columnar epithelium, when the healing of the lesion occurs. According to some studies, the incidence of the esophageal adenocarcinoma in patients with BE is of about 0,5% per year. The term Barrett's esophagus is subjected to interpretation nowadays, so it lacks the clarity needed for the clinical and scientific communication on the subject of columnar metaplasia of the esophageal mucosa. The major pathogenetic factor in the development of BE is represented by the reflux disease. The cellular origin of BE is controversial and it represents an issue that needs to be resolved because it will have implications in the putative molecular mechanisms underlying the metaplastic process. The epigenetic or genetic changes, which alter protein expression, function, and/ or activity, in post-mitotic cells to drive transdifferentiation or in stem/ progenitor cells such that they are reprogrammed to differentiate into columnar rather than squamous cells, are driven by the inflammatory environment created by chronic reflux. In order to be able to develop better therapeutic strategies for the patients with this disease, an increasing interest in understanding the pathogenesis of BE at the cellular and molecular level presents these days.

摘要

食管上皮损伤可能由胃酸反流至食管所决定。巴雷特食管(BE)的特征是在病变愈合时,正常鳞状上皮被柱状上皮取代。根据一些研究,BE患者中食管腺癌的发病率约为每年0.5%。如今,“巴雷特食管”这一术语存在多种解释,因此在关于食管黏膜柱状化生这一主题的临床和科学交流中缺乏所需的清晰度。BE发生发展的主要致病因素是反流性疾病。BE的细胞起源存在争议,这是一个需要解决的问题,因为它将对化生过程潜在的分子机制产生影响。慢性反流所产生的炎症环境驱动了后生细胞中的表观遗传或基因变化,这些变化改变蛋白质表达、功能和/或活性,以驱动转分化,或在干细胞/祖细胞中使其重新编程,从而分化为柱状而非鳞状细胞。为了能够为患有这种疾病的患者制定更好的治疗策略,如今人们越来越关注在细胞和分子水平上理解BE的发病机制。