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10.1073/pnas.1702750114

http://scihub22266oqcxt.onion/10.1073/pnas.1702750114
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C5422806!5422806!28416697
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suck abstract from ncbi


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pmid28416697      Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (18): 4679-84
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  • Small molecule-mediated inhibition of myofibroblast transdifferentiation for the treatment of fibrosis #MMPMID28416697
  • Bollong MJ; Yang B; Vergani N; Beyer BA; Chin EN; Zambaldo C; Wang D; Chatterjee AK; Lairson LL; Schultz PG
  • Proc Natl Acad Sci U S A 2017[May]; 114 (18): 4679-84 PMID28416697show ga
  • The treatment of fibrosis remains a critically important unmet medical need, as nearly 45% of all natural deaths in the Western world are attributed to chronic fibroproliferative disease complications. Fibrosis is characterized by the excessive deposition of extracellular matrix proteins by resident fibroblast-derived myofibroblasts. From an imaging-based screen, we identified the antifungal drug itraconazole as an inhibitor of myofibroblast transdifferentiation from multiple resident fibroblast populations. A derivative of this drug was found to inhibit fibrotic disease progression in mouse models of lung, liver, and skin fibrosis, demonstrating that inhibiting differentiation to the myofibroblast cell state is a practical strategy to treat a wide range of fibrosis-related diseases.
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