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@ARTICLE{Rohlfing:179481,
      author       = {A.-K. Rohlfing and K. Kolb and M. Sigle and M. Ziegler and
                      A. Bild and P. Münzer and J. Sudmann and V. Dicenta and T.
                      Harm and M.-C. Manke and S. Geue and M. Kremser and M.
                      Chatterjee and C. Liang and H. von Eysmondt and T. Dandekar
                      and D. Heinzmann and M. Günter$^*$ and S. von
                      Ungern-Sternberg and M. Büttcher and T. Castor and S. Mencl
                      and F. Langhauser and K. Sies$^*$ and D. Ashour and M. C.
                      Beker and M. Lämmerhofer and S. E. Autenrieth$^*$ and T. E.
                      Schäffer and S. Laufer and P. Szklanna and P. Maguire and
                      M. Heikenwalder$^*$ and K. A. L. Müller and D. M. Hermann
                      and E. Kilic and R. Stumm and G. Ramos and C. Kleinschnitz
                      and O. Borst and H. F. Langer and D. Rath and M. Gawaz},
      title        = {{ACKR}3 regulates platelet activation and
                      ischemia-reperfusion tissue injury.},
      journal      = {Nature Communications},
      volume       = {13},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2022-00695},
      pages        = {1823},
      year         = {2022},
      abstract     = {Platelet activation plays a critical role in thrombosis.
                      Inhibition of platelet activation is a cornerstone in
                      treatment of acute organ ischemia. Platelet ACKR3 surface
                      expression is independently associated with all-cause
                      mortality in CAD patients. In a novel genetic mouse strain,
                      we show that megakaryocyte/platelet-specific deletion of
                      ACKR3 results in enhanced platelet activation and thrombosis
                      in vitro and in vivo. Further, we performed
                      ischemia/reperfusion experiments (transient LAD-ligation and
                      tMCAO) in mice to assess the impact of genetic ACKR3
                      deficiency in platelets on tissue injury in ischemic
                      myocardium and brain. Loss of platelet ACKR3 enhances tissue
                      injury in ischemic myocardium and brain and aggravates
                      tissue inflammation. Activation of platelet-ACKR3 via
                      specific ACKR3 agonists inhibits platelet activation and
                      thrombus formation and attenuates tissue injury in ischemic
                      myocardium and brain. Here we demonstrate that ACKR3 is a
                      critical regulator of platelet activation, thrombus
                      formation and organ injury following ischemia/reperfusion.},
      keywords     = {Animals / Blood Platelets: metabolism / Humans / Mice /
                      Platelet Activation / Reperfusion / Reperfusion Injury:
                      genetics / Reperfusion Injury: metabolism / Thrombosis:
                      metabolism},
      cin          = {F171 / F180},
      ddc          = {500},
      cid          = {I:(DE-He78)F171-20160331 / I:(DE-He78)F180-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35383158},
      doi          = {10.1038/s41467-022-29341-1},
      url          = {https://inrepo02.dkfz.de/record/179481},
}