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@ARTICLE{DeAngelisRigotti:275423,
      author       = {F. De Angelis Rigotti$^*$ and L. Wiedmann$^*$ and M. O.
                      Hubert$^*$ and M. Vacca$^*$ and S. S. Hasan$^*$ and I.
                      Moll$^*$ and S. Carvajal and W. Jiménez and M.
                      Starostecka$^*$ and A. T. Billeter and B. Müller-Stich and
                      G. Wolff and B. Ekim-Üstünel and S. Herzig and C.
                      Fandos-Ramo and R. Krätzner and M. Reich and V.
                      Keitel-Anselmino and M. Heikenwälder$^*$ and C. Mogler and
                      A. Fischer and J. Rodriguez-Vita$^*$},
      title        = {{S}emaphorin 3{C} exacerbates liver fibrosis.},
      journal      = {Hepatology},
      volume       = {78},
      number       = {4},
      issn         = {0270-9139},
      address      = {New York [u.a.]},
      publisher    = {Wiley Interscience},
      reportid     = {DKFZ-2023-00746},
      pages        = {1092-1105},
      year         = {2023},
      note         = {#EA:A270#LA:A270# / 2023 Oct 1;78(4):1092-1105},
      abstract     = {Chronic liver disease is a growing epidemic, leading to
                      fibrosis and cirrhosis. TGF-β is the pivotal pro-fibrogenic
                      cytokine which activates hepatic stellate cells (HSC), yet,
                      other molecules can modulate TGF-β signaling during liver
                      fibrosis. Expression of the axon guidance molecules
                      Semaphorins (SEMAs), which signal through Plexins and
                      Neuropilins (NRPs), have been associated with liver fibrosis
                      in HBV-induced chronic hepatitis. This study aims at
                      determining their function in the regulation of HSCs. We
                      analyzed publicly available patient databases and liver
                      biopsies. We employed transgenic mice, in which genes are
                      deleted only in activated HSCs to perform ex vivo analysis
                      and animal models. SEMA3C is the most enriched member of the
                      Semaphorin family in liver samples from cirrhotic patients.
                      Higher expression of SEMA3C in patients with NASH, alcoholic
                      hepatitis or HBV-induced hepatitis discriminates those with
                      a more pro-fibrotic transcriptomic profile. SEMA3C
                      expression is also elevated in different mouse models of
                      liver fibrosis and in isolated HSCs upon activation. In
                      keeping with this, deletion of SEMA3C in activated HSCs
                      reduces myofibroblast marker expression. Conversely, SEMA3C
                      overexpression exacerbates TGF-β-mediated myofibroblast
                      activation, as shown by increased SMAD2 phosphorylation and
                      target gene expression. Among SEMA3C receptors, only NRP2
                      expression is maintained upon activation of isolated HSCs.
                      Interestingly, lack of NRP2 in those cells reduces
                      myofibroblast marker expression. Finally, deletion of either
                      SEMA3C or NRP2, specifically in activated HSCs, reduces
                      liver fibrosis in mice. SEMA3C is a novel marker for
                      activated HSCs that plays a fundamental role in the
                      acquisition of the myofibroblastic phenotype and liver
                      fibrosis.},
      cin          = {A270 / F180},
      ddc          = {610},
      cid          = {I:(DE-He78)A270-20160331 / I:(DE-He78)F180-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37055018},
      doi          = {10.1097/HEP.0000000000000407},
      url          = {https://inrepo02.dkfz.de/record/275423},
}