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@ARTICLE{Lux:141759,
      author       = {M. Lux and A. Blaut and N. Eltrich and A. Bideak and M. B.
                      Müller and J. M. Hoppe and H.-J. Gröne$^*$ and M. Locati
                      and V. Vielhauer},
      title        = {{T}he atypical chemokine receptor 2 limits progressive
                      fibrosis after acute ischemic kidney injury.},
      journal      = {The American journal of pathology},
      volume       = {189},
      number       = {2},
      issn         = {0002-9440},
      address      = {New York [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2018-02028},
      pages        = {231-247},
      year         = {2019},
      abstract     = {Following renal ischemia-reperfusion injury (IRI)
                      resolution of inflammation allows tubular regeneration,
                      whereas ongoing inflammatory injury mediated by infiltrating
                      leukocytes leads to nephron loss and renal fibrosis, typical
                      hallmarks of chronic kidney disease. The atypical chemokine
                      receptor 2 (ACKR2) is a chemokine decoy receptor, that binds
                      and scavenges inflammatory CC-chemokines and reduces local
                      leukocyte accumulation. We hypothesized that ACKR2 limits
                      leukocyte infiltration, inflammation, and fibrotic tissue
                      remodeling after renal IRI, thus preventing progression to
                      chronic kidney disease. Compared to wild-type, Ackr2
                      deficiency increased CC chemokine ligand 2 levels in tumor
                      necrosis factor-stimulated tubulointerstitial tissue in
                      vitro. In Ackr2-deficient mice with early IRI one or five
                      days after transient renal pedicle clamping tubular injury
                      was similar to wild-type, although accumulation of
                      mononuclear phagocytes increased in postischemic Ackr2-/-
                      kidneys. Regarding long-term outcomes, Ackr2-/- kidneys
                      displayed more tubular injury five weeks after IRI, which
                      was associated with persistently increased renal infiltrates
                      of mononuclear phagocytes, T cells, Ly6Chigh inflammatory
                      macrophages, and inflammation. Moreover, Ackr2 deficiency
                      resulted in substantially aggravated renal fibrosis in
                      Ackr2-/- kidneys five weeks after IRI, as revealed by
                      increased expression of matrix molecules, renal accumulation
                      of αSMA+ myofibroblasts, and bone marrow-derived
                      fibrocytes. ACKR2 plays an important role in limiting
                      persistent inflammation, tubular loss, and renal fibrosis
                      after ischemic acute kidney injury, and thus can prevent
                      progression to chronic renal disease.},
      cin          = {G130},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30448408},
      doi          = {10.1016/j.ajpath.2018.09.016},
      url          = {https://inrepo02.dkfz.de/record/141759},
}