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