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Rheumatology Advance Access originally published online on November 23, 2008
Rheumatology 2009 48(1):2-4; doi:10.1093/rheumatology/ken431
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

EDITORIALS

Imatinib as a novel therapeutic approach for fibrotic disorders

J. H. W. Distler1 and O. Distler2

1Department of Internal Medicine III, University of Erlangen-Nuremberg, Bavaria, Germany and 2Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland

Correspondence to: O. Distler, Department of Rheumatology, University Hospital Zurich, Gloriastr. 25, CH-8091 Zurich, Switzerland. E-mail: Oliver.Distler@usz.ch

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

Imatinib mesylate is a small molecule that binds to the ATP-binding pocket of Abelson kinase (c-Abl) and blocks efficiently its tyrosine kinase activity. c-Abl is an important downstream signalling molecule of TGF-β [1]. The importance of c-Abl for the pro-fibrotic effects of TGF-β is emphasized by the observation that the induction of extracellular matrix proteins by TGF-β is strongly decreased in cells deficient for c-Abl. In addition to its effects on c-Abl, imatinib blocks the tyrosine kinase activity of PDGF receptors. Thus, imatinib targets simultaneously and also rather selectively TGF-β and PDGF signalling, two major pro-fibrotic pathways in SSc [2].

Imatinib is widely used for the treatment of bcr-Abl-positive chronic myelogenous leukaemia (CML) and gastrointestinal stromal tumours with more than 100 000 patients treated so far. Imatinib possesses favourable pharmacokinetics: (i) it is readily absorbed after oral administration; (ii) one dose per day is sufficient, because . . . [Full Text of this Article]

Pre-clinical evidence for the anti-fibrotic effects of imatinib

Clinical outcome of first patients with fibrotic diseases

Conclusions


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