We are analyzing https://link.springer.com/article/10.1007/s00403-012-1304-7.

Title:
Morphogen pathways as molecular targets for the treatment of fibrosis in systemic sclerosis | Archives of Dermatological Research
Description:
Wnt-, Hedgehog- and Notch-signaling cascades are morphogen pathways that play crucial roles in development and tissue homeostasis. While morphogen pathways are tightly regulated at multiple levels, inappropriate activation of Wnt, Hedgehog and Notch signaling has been implicated into the pathogenesis of various diseases. In particular, Wnt, Hedgehog and Notch signaling have emerged as central players in the pathogenesis of fibrotic diseases. Here, we will review the pro-fibrotic effects of Wnt, Hedgehog and Notch signaling in systemic sclerosis (SSc), prototypical systemic fibrotic disease. Wnt, Hedgehog and Notch pathways are activated in SSc. They potently stimulate fibroblasts to differentiate into myofibroblasts and to release collagen and other extracellular matrix components. Genetic or pharmacological inhibition of morphogen pathways effectively prevents experimental fibrosis in different preclinical models and induces regression of pre-established fibrosis. As several inhibitors of Wnt, Hedgehog and Notch have recently been developed with first ones being already approved for clinical trials, morphogen pathways maybe a novel approach for the treatment of fibrosis.
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Keywords {🔍}

article, google, scholar, pubmed, cas, distler, signaling, fibrosis, systemic, sclerosis, wnt, notch, beyer, hedgehog, cell, dees, biol, rheum, schett, pathways, signalling, morphogen, activation, inhibition, akhmetshina, zerr, ann, dis, research, induces, access, canonical, dermatol, privacy, cookies, content, treatment, development, disease, experimental, palumbo, horn, zwerina, nat, dev, tomcik, arthritis, sato, arch, res,

Topics {✒️}

month download article/chapter tgf-beta-mediated fibrosis wnt/beta-catenin signaling functional gamma-secretase inhibitor sap18-msin3 corepressor complex canonical wnt signalling 1007/s00403-012-1292-7 yanaba pro-fibrotic wnt signaling notch-mediated transcriptional switch drugging wnt signalling related subjects reduces experimental fibrosis full article pdf wnt signaling pathways canonical wnt pathway idiopathic pulmonary fibrosis gamma-secretase inhibitors privacy choices/manage cookies human dermal fibroblasts hedgehog signalling hedgehog-gli pathway notch-signaling cascades modulating notch signaling activate notch signaling soluble inducible costimulator canonical notch ligands dermatological research aims van den born pulmonary arterial hypertension pro-fibrotic effects gastrointestinal toxicity mediated author correspondence notch ligands dll1 beta-catenin pre-established fibrosis check access instant access article beyer tsk mouse skin european economic area play crucial roles potently stimulate fibroblasts innovative antifibrotic therapies mora-blanco el goblet cells mesenchymal cells ankyrin repeat domain homeostatic stem cell arch dermatol res morphogen pathways

Questions {❓}

Wei J, Melichian D, Komura K, Hinchcliff M, Lam AP, Lafyatis R, Gottardi CJ, MacDougald OA, Varga J (2011) Canonical Wnt signaling induces skin fibrosis and subcutaneous lipoatrophy: a novel mouse model for scleroderma?

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      headline:Morphogen pathways as molecular targets for the treatment of fibrosis in systemic sclerosis
      description:Wnt-, Hedgehog- and Notch-signaling cascades are morphogen pathways that play crucial roles in development and tissue homeostasis. While morphogen pathways are tightly regulated at multiple levels, inappropriate activation of Wnt, Hedgehog and Notch signaling has been implicated into the pathogenesis of various diseases. In particular, Wnt, Hedgehog and Notch signaling have emerged as central players in the pathogenesis of fibrotic diseases. Here, we will review the pro-fibrotic effects of Wnt, Hedgehog and Notch signaling in systemic sclerosis (SSc), prototypical systemic fibrotic disease. Wnt, Hedgehog and Notch pathways are activated in SSc. They potently stimulate fibroblasts to differentiate into myofibroblasts and to release collagen and other extracellular matrix components. Genetic or pharmacological inhibition of morphogen pathways effectively prevents experimental fibrosis in different preclinical models and induces regression of pre-established fibrosis. As several inhibitors of Wnt, Hedgehog and Notch have recently been developed with first ones being already approved for clinical trials, morphogen pathways maybe a novel approach for the treatment of fibrosis.
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