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Orphan nuclear receptor NR4A1 regulates transforming growth factor-beta signaling and fibrosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F15%3A10294722" target="_blank" >RIV/00216208:11110/15:10294722 - isvavai.cz</a>

  • Alternative codes found

    RIV/00023728:_____/15:#0005052

  • Result on the web

    <a href="http://dx.doi.org/10.1038/nm.3777" target="_blank" >http://dx.doi.org/10.1038/nm.3777</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/nm.3777" target="_blank" >10.1038/nm.3777</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Orphan nuclear receptor NR4A1 regulates transforming growth factor-beta signaling and fibrosis

  • Original language description

    Mesenchymal responses are an essential aspect of tissue repair. Failure to terminate this repair process correctly, however, results in fibrosis and organ dysfunction. Therapies that block fibrosis and restore tissue homeostasis are not yet available forclinical use. Here we characterize the nuclear receptor NR4A1 as an endogenous inhibitor of transforming growth factor-beta (TGF-beta) signaling and as a potential target for anti-fibrotic therapies. NR4A1 recruits a repressor complex comprising SP1, SIN3A, CoREST, LSD1, and HDAC1 to TGF-beta target genes, thereby limiting pro-fibrotic TGF-beta effects. Even though temporary upregulation of TGF-beta in physiologic wound healing induces NR4A1 expression and thereby creates a negative feedback loop, thepersistent activation of TGF-beta signaling in fibrotic diseases uses AKT- and HDAC-dependent mechanisms to inhibit NR4A1 expression and activation. Small-molecule NR4A1 agonists can overcome this lack of active NR4A1 and inhibit experime

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    FE - Other fields of internal medicine

  • OECD FORD branch

Result continuities

  • Project

  • Continuities

    S - Specificky vyzkum na vysokych skolach

Others

  • Publication year

    2015

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Nature Medicine

  • ISSN

    1078-8956

  • e-ISSN

  • Volume of the periodical

    21

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    9

  • Pages from-to

    150-158

  • UT code for WoS article

    000348974800017

  • EID of the result in the Scopus database

    2-s2.0-84925537240