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@ARTICLE{Lam:296114,
      author       = {W. M. Lam$^*$ and G. Gabernet and T. Poth and M.
                      Sator-Schmitt$^*$ and M. B. Oquendo and B. Walter$^*$ and S.
                      Lohr$^*$ and A. De Ponti$^*$ and L. Weiß$^*$ and M.
                      Schneider$^*$ and D. Helm$^*$ and K. Müller-Decker$^*$ and
                      P. Schirmacher and M. Heikenwälder$^*$ and U.
                      Klingmüller$^*$ and D. Schneller$^*$ and F. Geisler and S.
                      Nahnsen and P. Angel$^*$},
      title        = {{RAGE} is a key regulator of ductular reaction-mediated
                      fibrosis during cholestasis.},
      journal      = {EMBO reports},
      volume       = {26},
      number       = {3},
      issn         = {1469-221X},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2025-00044},
      pages        = {880-907},
      year         = {2025},
      note         = {DKFZ-ZMBH Alliance / 2025 Feb;26(3):880-907 /
                      #EA:A100#LA:A100#},
      abstract     = {Ductular reaction (DR) is the hallmark of cholestatic
                      diseases manifested in the proliferation of bile ductules
                      lined by biliary epithelial cells (BECs). It is commonly
                      associated with an increased risk of fibrosis and liver
                      failure. The receptor for advanced glycation end products
                      (RAGE) was identified as a critical mediator of DR during
                      chronic injury. Yet, the direct link between RAGE-mediated
                      DR and fibrosis as well as the mode of interaction between
                      BECs and hepatic stellate cells (HSCs) to drive fibrosis
                      remain elusive. Here, we delineate the specific function of
                      RAGE on BECs during DR and its potential association with
                      fibrosis in the context of cholestasis. Employing a biliary
                      lineage tracing cholestatic liver injury mouse model,
                      combined with whole transcriptome sequencing and in vitro
                      analyses, we reveal a role for BEC-specific Rage activity in
                      fostering a pro-fibrotic milieu. RAGE is predominantly
                      expressed in BECs and contributes to DR. Notch ligand
                      Jagged1 is secreted from activated BECs in a Rage-dependent
                      manner and signals HSCs in trans, eventually enhancing
                      fibrosis during cholestasis.},
      keywords     = {Biliary Epithelial Cells (Other) / Chronic Liver Injury
                      (Other) / Genetically Modified Mice (Other) / Hepatic
                      Stellate Cells (Other) / Receptor for Advanced Glycation End
                      Products (Other)},
      cin          = {A100 / W120 / W420 / D440 / B200},
      ddc          = {570},
      cid          = {I:(DE-He78)A100-20160331 / I:(DE-He78)W120-20160331 /
                      I:(DE-He78)W420-20160331 / I:(DE-He78)D440-20160331 /
                      I:(DE-He78)B200-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39747668},
      doi          = {10.1038/s44319-024-00356-7},
      url          = {https://inrepo02.dkfz.de/record/296114},
}