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@ARTICLE{Anisimov:277772,
      author       = {A. Anisimov and S. Fang and K. A. Hemanthakumar and T. Örd
                      and K. van Avondt and R. Chevre and A. Toropainen and P.
                      Singha and H. Gilani and S. D. Nguyen and S. Karaman and E.
                      A. Korhonen and R. H. Adams and H. Augustin$^*$ and K.
                      Öörni and O. Soehnlein and M. U. Kaikkonen and K. Alitalo},
      title        = {{T}he angiopoietin receptor {T}ie2 is atheroprotective in
                      arterial endothelium.},
      journal      = {Nature cardiovascular research},
      volume       = {2},
      number       = {3},
      issn         = {2731-0590},
      address      = {London},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-01487},
      pages        = {307 - 321},
      year         = {2023},
      abstract     = {Leukocytes and resident cells in the arterial wall
                      contribute to atherosclerosis, especially at sites of
                      disturbed blood flow. Expression of endothelial Tie1
                      receptor tyrosine kinase is enhanced at these sites, and
                      attenuation of its expression reduces atherosclerotic burden
                      and decreases inflammation. However, Tie2 tyrosine kinase
                      function in atherosclerosis is unknown. Here we provide
                      genetic evidence from humans and from an atherosclerotic
                      mouse model to show that TIE2 is associated with protection
                      from coronary artery disease. We show that deletion of Tie2,
                      or both Tie2 and Tie1, in the arterial endothelium promotes
                      atherosclerosis by increasing Foxo1 nuclear localization,
                      endothelial adhesion molecule expression and accumulation of
                      immune cells. We also show that Tie2 is expressed in a
                      subset of aortic fibroblasts, and its silencing in these
                      cells increases expression of inflammation-related genes.
                      Our findings indicate that unlike Tie1, the Tie2 receptor
                      functions as the dominant endothelial angiopoietin receptor
                      that protects from atherosclerosis.},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37476204},
      pmc          = {pmc:PMC7614785},
      doi          = {10.1038/s44161-023-00224-y},
      url          = {https://inrepo02.dkfz.de/record/277772},
}