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@ARTICLE{Willenborg:163396,
      author       = {Willenborg, Sebastian and Sanin, David E and Jais,
                      Alexander and Ding, Xiaolei and Ulas, Thomas and Nüchel,
                      Julian and Popović, Milica and MacVicar, Thomas and Langer,
                      Thomas and Schultze, Joachim L and Gerbaulet, Alexander and
                      Roers, Axel and Pearce, Edward J and Brüning, Jens C and
                      Trifunovic, Aleksandra and Eming, Sabine A},
      title        = {{M}itochondrial metabolism coordinates stage-specific
                      repair processes in macrophages during wound healing.},
      journal      = {Cell metabolism},
      volume       = {33},
      number       = {12},
      issn         = {1550-4131},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DZNE-2022-00158},
      pages        = {2398 - 2414.e9},
      year         = {2021},
      note         = {(CC BY)},
      abstract     = {Wound healing is a coordinated process that initially
                      relies on pro-inflammatory macrophages, followed by a
                      pro-resolution function of these cells. Changes in cellular
                      metabolism likely dictate these distinct activities, but the
                      nature of these changes has been unclear. Here, we profiled
                      early- versus late-stage skin wound macrophages in mice at
                      both the transcriptional and functional levels. We found
                      that glycolytic metabolism in the early phase is not
                      sufficient to ensure productive repair. Instead, by
                      combining conditional disruption of the electron transport
                      chain with deletion of mitochondrial aspartyl-tRNA
                      synthetase, followed by single-cell sequencing analysis, we
                      found that a subpopulation of early-stage wound macrophages
                      are marked by mitochondrial ROS (mtROS) production and
                      HIF1α stabilization, which ultimately drives a
                      pro-angiogenic program essential for timely healing. In
                      contrast, late-phase, pro-resolving wound macrophages are
                      marked by IL-4Rα-mediated mitochondrial respiration and
                      mitohormesis. Collectively, we identify changes in
                      mitochondrial metabolism as a critical control mechanism for
                      macrophage effector functions during wound healing.},
      keywords     = {Animals / Macrophages: metabolism / Mice / Mitochondria:
                      metabolism / Wound Healing / metabolism (Other) /
                      mitochondria (Other) / mitochondrial repurposing (Other) /
                      mitohormesis (Other) / monocyte/macrophage (Other) / tissue
                      repair (Other) / type 2 immunity (Other) / wound healing
                      (Other)},
      cin          = {AG Schultze},
      ddc          = {570},
      cid          = {I:(DE-2719)1013031},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34715039},
      doi          = {10.1016/j.cmet.2021.10.004},
      url          = {https://pub.dzne.de/record/163396},
}