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Showing 1–4 of 4 results
Advanced filters: Author: Clara Dees Clear advanced filters

  • The transcription factor PU.1 is an essential regulator of the pro-fibrotic gene expression program in fibroblasts; PU.1 expression is upregulated in various fibrotic diseases, whereas inactivation of PU.1 induces regression of fibrosis in a number of organs.

    • Thomas Wohlfahrt
    • Simon Rauber
    • Andreas Ramming
    Research
    Nature
    Volume: 566, P: 344-349

  • Aberrant activation of the TGF-β pathway leads to fibrotic disease. Distler and colleagues show that TGF-β-mediated fibrosis requires the decrease of Dickkopf-1, an antagonist of canonical Wnt signalling, suggesting that the two pathways interact for the manifestation of this disease.

    • Alfiya Akhmetshina
    • Katrin Palumbo
    • Jörg H.W. Distler
    ResearchOpen Access
    Nature Communications
    Volume: 3, P: 1-12

  • Hyperactivation of TGFβ signaling is a common feature of fibrotic diseases. Here the authors show that genetic or pharmacologic inactivation of the tyrosine phosphatase SHP2 prevents TGFβ-induced JAK2/STAT3 signaling, inhibits fibroblast activation and exerts potent anti-fibrotic effects.

    • Ariella Zehender
    • Jingang Huang
    • Jörg H. W. Distler
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-17