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Gut 2009;58:i-ii
Copyright © 2009 BMJ Publishing Group Ltd & British Society of Gastroenterology.

Digest

Digest

Robin Spiller, Magnus Simren, editor and deputy editor

The first 150 words of the full text of this article appear below.

Imbalance between deposition of extracellular matrix and its degradation in Crohn’s strictures

Fibrosis in inflammatory bowel disease is believed to be due to an excess deposition of extracellular matrix (ECM) by myofibroblasts and an impairment of the matrix degrading metalloproteinases (MMPs). Transforming growth factor-β (TGFβ) stimulates ECM synthesis and the level of MMPs are reduced by tissue inhibitors of metalloproteinase (TIMPs). This study examined uninflamed mucosa from 25 patients with Crohn’s disease (CD) with strictures and compared this with tissue from 18 patients with CD without stricturing. TGFβ was over expressed in myofibroblasts from mucosa overlying strictures (see fig). Binding of TGF activates the Smad proteins, phosphorylating Smad 2 and 3 whose action on gene transcription is inhibited by Smad 6 and 7. The authors showed an increase in phosphorylated Smad 2 and 3 from mucosa above the stricture and a decrease in the inhibitory Smad 6 and 7. There was also a reduction in mucosal MMP-12 and an increase in the . . . [Full text of this article]


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