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@ARTICLE{Rodrigues:136792,
      author       = {R. M. Rodrigues and L. Kollipara and U. Chaudhari and A.
                      Sachinidis and R. P. Zahedi and A. Sickmann and A.
                      Kopp-Schneider$^*$ and X. Jiang$^*$ and H. Keun and J.
                      Hengstler and M. Oorts and P. Annaert and E. Hoeben and E.
                      Gijbels and J. De Kock and T. Vanhaecke and V. Rogiers and
                      M. Vinken},
      title        = {{O}mics-based responses induced by bosentan in human
                      hepatoma {H}epa{RG} cell cultures.},
      journal      = {Archives of toxicology},
      volume       = {92},
      number       = {6},
      issn         = {1432-0738},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DKFZ-2018-01230},
      pages        = {1939 - 1952},
      year         = {2018},
      abstract     = {Bosentan is well known to induce cholestatic liver toxicity
                      in humans. The present study was set up to characterize the
                      hepatotoxic effects of this drug at the transcriptomic,
                      proteomic, and metabolomic levels. For this purpose, human
                      hepatoma-derived HepaRG cells were exposed to a number of
                      concentrations of bosentan during different periods of time.
                      Bosentan was found to functionally and transcriptionally
                      suppress the bile salt export pump as well as to alter bile
                      acid levels. Pathway analysis of both transcriptomics and
                      proteomics data identified cholestasis as a major
                      toxicological event. Transcriptomics results further showed
                      several gene changes related to the activation of the
                      nuclear farnesoid X receptor. Induction of oxidative stress
                      and inflammation were also observed. Metabolomics analysis
                      indicated changes in the abundance of specific endogenous
                      metabolites related to mitochondrial impairment. The outcome
                      of this study may assist in the further optimization of
                      adverse outcome pathway constructs that mechanistically
                      describe the processes involved in cholestatic liver
                      injury.},
      cin          = {C060},
      ddc          = {610},
      cid          = {I:(DE-He78)C060-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29761207},
      doi          = {10.1007/s00204-018-2214-z},
      url          = {https://inrepo02.dkfz.de/record/136792},
}