Smad3 as a mediator of the fibrotic response
By K. Flanders. International journal of experimental pathology (Print), 2004
661 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/fd62cf997e463f72394a47acc354740c12c469f6
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In Molecular Biology
- A. Moustakas
- C. Heldin
- J. Sleeman
- J. P. Thiery
- Jiri Zavadil
- Brigham C. Willis
- Erwin P. Bottinger
- Ralf Weiskirchen
Citations in the corpus
- TGF-β and epithelial-to-mesenchymal transitions (2005, background): “The role of Smad3 in EMT and fibrosis has been extensively reviewed recently (Flanders, 2004).”
- TGF-β-induced EMT: mechanisms and implications for fibrotic lung disease (2007, background): “EMT in response to TGF- 1 and in fibrosis is mediated predominantly via Smad-dependent (mainly Smad3) pathways, although as discussed further below, non-Smad signaling has also been implicated under certain circumstances (20).”
- Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets (2006, background): “Hence, given the prominent role of Smad3 in mediating the pathobiology of fibrotic diseases, inhibition of Smad3 signalling could be a prime target for intervention in fibrotic conditions (for review see [57]).”
- The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “Agents that target specific pathways downstream of the TGF-β receptor are more likely to have the desired effects while avoiding unwanted complications [ 87 ].”
- Non-Smad TGF-β signals (2005, background): “Thus, whereas specific inhibitors of Smad3 have been emphasized for the treatment of tumour metastasis (Flanders, 2004), a combination of Smad inhibitors and kinase or GTPase inhibitors may be more efficacious.”
- Complex networks orchestrate epithelial–mesenchymal transitions (2006, background): “The recurring theme of the involvement of TGFβ in the pathogenesis of EMT-dependent fibrotic diseases is highlighted by the finding that Smad3 −/− mice are resistant to the induction of several fibrotic disease”