Fxr-deficiency in mouse liver slices aggravates cyclosporin A toxicity by upregulation of pro-inflammatory genes and downregulation of genes involved in mitochondrial functions



    The transcription factor farnesoid X receptor (FXR) governs bile acid and energy homeostasis, is involved in inflammation, and has protective functions in the liver. In the present study we investigated the effect of Fxr deficiency in mouse precision cut liver slices (PCLS) exposed to a model hepatotoxicant cyclosporin A (CsA). It was anticipated that Fxr deficiency could aggravate toxicity of CsA in PCLS and pinpoint to novel genes/processes regulated by FXR.
    Date made available22 Oct 2015
    PublisherRIKILT Wageningen UR


    • Mus musculus

    Accession numbers

    • GSE63457
    • PRJNA267834

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