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@ARTICLE{Ortiz:1005353,
      author       = {Ortiz, Cristina and Klein, Sabine and Reul, Winfried H. and
                      Magdaleno, Fernando and Gröschl, Stefanie and Dietrich,
                      Peter and Schierwagen, Robert and Uschner, Frank E. and
                      Torres, Sandra and Hieber, Christoph and Meier, Caroline and
                      Kraus, Nico and Tyc, Olaf and Brol, Maximilian and Zeuzem,
                      Stefan and Welsch, Christoph and Poglitsch, Marco and
                      Hellerbrand, Claus and Alfonso-Prieto, Mercedes and Mira,
                      Fabio and Keller, Ulrich auf dem and Tetzner, Anja and
                      Moore, Andrew and Walther, Thomas and Trebicka, Jonel},
      title        = {{N}eprilysin-dependent neuropeptide {Y} cleavage in the
                      liver promotes fibrosis by blocking {NPY}-receptor 1},
      journal      = {Cell reports},
      volume       = {42},
      number       = {2},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2023-01456},
      pages        = {112059},
      year         = {2023},
      abstract     = {Development of liver fibrosis is paralleled by contraction
                      of hepatic stellate cells (HSCs), the main profibrotic
                      hepatic cells. Yet, little is known about the interplay of
                      neprilysin (NEP) and its substrate neuropeptide Y (NPY), a
                      potent enhancer of contraction, in liver fibrosis. We
                      demonstrate that HSCs are the source of NEP. Importantly,
                      NPY originates majorly from the splanchnic region and is
                      cleaved by NEP in order to terminate contraction.
                      Interestingly, NEP deficiency (Nep−/−) showed less
                      fibrosis but portal hypertension upon liver injury in two
                      different fibrosis models in mice. We demonstrate the
                      incremental benefit of Nep−/− in addition to AT1R
                      blocker (ARB) or ACE inhibitors for fibrosis and portal
                      hypertension. Finally, oral administration of Entresto, a
                      combination of ARB and NEP inhibitor, decreased hepatic
                      fibrosis and portal pressure in mice. These results provide
                      a mechanistic rationale for translation of NEP-AT1R-blockade
                      in human liver fibrosis and portal hypertension.},
      cin          = {IAS-5 / INM-9},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121},
      pnm          = {5241 - Molecular Information Processing in Cellular Systems
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5241},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {36729833},
      UT           = {WOS:000927805600001},
      doi          = {10.1016/j.celrep.2023.112059},
      url          = {https://juser.fz-juelich.de/record/1005353},
}