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食管柱状化生或巴雷特食管发病机制的新发现。

Novel findings in the pathogenesis of esophageal columnar metaplasia or Barrett's esophagus.

作者信息

Krishnadath Kausilia K

机构信息

Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.

出版信息

Curr Opin Gastroenterol. 2007 Jul;23(4):440-5. doi: 10.1097/MOG.0b013e32814e6b4f.

DOI:10.1097/MOG.0b013e32814e6b4f
PMID:17545783
Abstract

PURPOSE OF REVIEW

In esophageal metaplasia the transdifferentiation of the epithelium is the result of longstanding gastroesophageal reflux disease that causes inflammation of the esophageal squamous mucosa, and occasionally is followed by replacement of the squamous epithelium by a columnar type of mucosa. For a long time, the molecular mechanisms involved in metaplasia were poorly understood. This review focuses on several recent findings on the molecular mechanisms involved in esophageal columnar metaplasia.

RECENT FINDINGS

Our recent findings on bone morphogenetic protein 4 and other recent discoveries in the field of cell signaling that take place during the sequence of inflammation and epithelial transdifferentiation are highlighted. In this process, several embryonic pathways that were silenced in the adult esophagus, and factors that are normally involved in the homeostasis of the large intestine, seem to be induced. These factors may mediate transdifferentiation of the esophageal epithelium.

SUMMARY

Although there are many aspects that need further investigation, it seems that in columnar metaplasia of the esophagus inductive morphogenes such as bone morphogenetic protein 4 are important for development and differentiation. Development of specialized intestinal type of metaplasia is the result of a succession of events, in which the effect of stromal factors is followed by expression of intestine-specific factors.

摘要

综述目的

在食管化生过程中,上皮的转分化是长期胃食管反流病导致食管鳞状黏膜炎症的结果,偶尔会继之以柱状黏膜取代鳞状上皮。长期以来,化生所涉及的分子机制一直未被充分理解。本综述聚焦于食管柱状化生所涉及分子机制的几项最新研究发现。

最新研究发现

重点介绍了我们关于骨形态发生蛋白4的最新研究发现以及该领域在炎症和上皮转分化过程中发生的细胞信号传导方面的其他最新发现。在此过程中,一些在成年食管中沉默的胚胎途径以及通常参与大肠稳态的因子似乎被诱导。这些因子可能介导食管上皮的转分化。

总结

尽管有许多方面需要进一步研究,但在食管柱状化生中,诸如骨形态发生蛋白4之类的诱导性形态发生素似乎对发育和分化很重要。特殊肠化生类型的发展是一系列事件的结果,其中基质因子的作用之后是肠特异性因子的表达。

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