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@ARTICLE{Kim:154376,
      author       = {J. Kim and J. R. Park and J. Choi and I. Park and Y. Hwang
                      and H. Bae and Y. Kim and W. Choi and J. M. Yang and S. Han
                      and T.-Y. Chung and P. Kim and Y. Kubota and H. Augustin$^*$
                      and W.-Y. Oh and G. Y. Koh},
      title        = {{T}ie2 activation promotes choriocapillary regeneration for
                      alleviating neovascular age-related macular degeneration.},
      journal      = {Science advances},
      volume       = {5},
      number       = {2},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2020-00716},
      pages        = {eaau6732 -},
      year         = {2019},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Choriocapillary loss is a major cause of neovascular
                      age-related macular degeneration (NV-AMD). Although vascular
                      endothelial growth factor (VEGF) blockade for NV-AMD has
                      shown beneficial outcomes, unmet medical needs for patients
                      refractory or tachyphylactic to anti-VEGF therapy exist. In
                      addition, the treatment could exacerbate choriocapillary
                      rarefaction, necessitating advanced treatment for
                      fundamental recovery from NV-AMD. In this study, Tie2
                      activation by angiopoietin-2-binding and Tie2-activating
                      antibody (ABTAA) presents a therapeutic strategy for NV-AMD.
                      Conditional Tie2 deletion impeded choriocapillary
                      maintenance, rendering eyes susceptible to NV-AMD
                      development. Moreover, in a NV-AMD mouse model, ABTAA not
                      only suppressed choroidal neovascularization (CNV) and
                      vascular leakage but also regenerated the choriocapillaris
                      and relieved hypoxia. Conversely, VEGF blockade degenerated
                      the choriocapillaris and exacerbated hypoxia, although it
                      suppressed CNV and vascular leakage. Together, we establish
                      that angiopoietin-Tie2 signaling is critical for
                      choriocapillary maintenance and that ABTAA represents an
                      alternative, combinative therapeutic strategy for NV-AMD by
                      alleviating anti-VEGF adverse effects.},
      keywords     = {Angiopoietin-1 (NLM Chemicals) / Angpt1 protein, mouse (NLM
                      Chemicals) / Vascular Endothelial Growth Factor A (NLM
                      Chemicals) / Receptor, TIE-2 (NLM Chemicals) / Tek protein,
                      mouse (NLM Chemicals)},
      cin          = {A190},
      ddc          = {500},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30788433},
      pmc          = {pmc:PMC6374104},
      doi          = {10.1126/sciadv.aau6732},
      url          = {https://inrepo02.dkfz.de/record/154376},
}