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. 2011 Jun 28;4:14. doi: 10.1186/1755-1536-4-14

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Copyright ©2011 Krause et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Schematic representation of perturbed TGF-β/Smad and mitogen-activated protein kinase signalling pathways in Dupuytren's fibroblasts. The TGF-β/Smad canonical Smad2/3 pathway and the noncanonical ERK1/2 mitogen-activated protein (MAP) kinase signalling pathways are depicted, as well as the PDGF-induced Ras/Raf/MEK/ERK1/2/MAP kinase pathway. TGF-β induces the production of PDGF and other growth factors. The symbols of corresponding downstream regulated genes are shown in italics. Inhibition by STI571, SB-431542 and PD98059 of the aberrantly overactivated signalling pathways in Dupuytren's fibroblasts is indicated. The mechanism by which BMP6 inhibits TGF-β expression and downstream responses is unclear. SB-431542 inhibits not only TGF-β/activin receptor-like kinase 5 (ALK5) signalling but also activin/ALK4 and nodal/ALK7 signalling. Our experiments do not rule out a role for these signalling pathways in Dupuytren's fibroblasts. Our data suggest that the TGF-β/Smad and PDGF/ERK MAP kinase pathways are targets for therapeutic intervention strategies to treat DD.