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Phenotypic drug screening in a human fibrosis model identified a novel class of antifibrotic therapeutics

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    SYSNO ASEP0554604
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitlePhenotypic drug screening in a human fibrosis model identified a novel class of antifibrotic therapeutics
    Author(s) Gerckens, M. (DE)
    Sarnová, Lenka (UMG-J)
    Jiroušková, Markéta (UMG-J) RID, ORCID
    Gregor, Martin (UMG-J) RID, ORCID
    Burgstaller, G. (DE)
    Number of authors30
    Article numbereabb3673
    Source TitleScience Advances. - : American Association for the Advancement of Science - ISSN 2375-2548
    Roč. 7, č. 52 (2021)
    Number of pages19 s.
    Publication formOnline - E
    Languageeng - English
    CountryUS - United States
    Keywordsidiopathic pulmonary-fibrosis ; growth-factor-beta ; selective-inhibition ; acute exacerbation ; label-free ; proteome ; matrix ; trial ; mechanisms ; tranilast
    Subject RIVEB - Genetics ; Molecular Biology
    OECD categoryCell biology
    R&D ProjectsNV17-31538A GA MZd - Ministry of Health (MZ)
    LQ1604 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    GA18-02699S GA ČR - Czech Science Foundation (CSF)
    Method of publishingOpen access
    Institutional supportUMG-J - RVO:68378050
    UT WOS000733258700009
    DOI10.1126/sciadv.abb3673
    AnnotationFibrogenic processes instigate fatal chronic diseases leading to organ failure and death. Underlying biological processes involve induced massive deposition of extracellular matrix (ECM) by aberrant fibroblasts. We subjected diseased primary human lung fibroblasts to an advanced three-dimensional phenotypic high-content assay and screened a repurposing drug library of small molecules for inhibiting ECM deposition. Fibrotic Pattern Detection by Artificial Intelligence identified tranilast as an effective inhibitor. Structure-activity relationship studies confirmed N-(2-butoxyphenyl)-3-(phenyl)acrylamides (N23Ps) as a novel and highly potent compound class. N23Ps suppressed myofibroblast transdifferentiation, ECM deposition, cellular contractility, and altered cell shapes, thus advocating a unique mode of action. Mechanistically, transcriptomics identified SMURF2 as a potential therapeutic target network. Antifibrotic activity of N23Ps was verified by proteomics in a human ex vivo tissue fibrosis disease model, suppressing profibrotic markers SERPINE1 and CXCL8. Conclusively, N23Ps are a novel class of highly potent compounds inhibiting organ fibrosis in patients.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2022
    Electronic addresshttps://www.science.org/doi/10.1126/sciadv.abb3673
Number of the records: 1  

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