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@ARTICLE{Motori:137156,
      author       = {Motori, Elisa and Puyal, Julien and Toni, Nicolas and
                      Ghanem, Alexander and Angeloni, Cristina and Malaguti, Marco
                      and Cantelli-Forti, Giorgio and Berninger, Benedikt and
                      Conzelmann, Karl-Klaus and Götz, Magdalena and Winklhofer,
                      Konstanze F and Hrelia, Silvana and Bergami, Matteo},
      title        = {{I}nflammation-induced alteration of astrocyte
                      mitochondrial dynamics requires autophagy for mitochondrial
                      network maintenance.},
      journal      = {Cell metabolism},
      volume       = {18},
      number       = {6},
      issn         = {1550-4131},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DZNE-2020-03478},
      pages        = {844-859},
      year         = {2013},
      abstract     = {Accumulating evidence suggests that changes in the
                      metabolic signature of astrocytes underlie their response to
                      neuroinflammation, but how proinflammatory stimuli induce
                      these changes is poorly understood. By monitoring astrocytes
                      following acute cortical injury, we identified a
                      differential and region-specific remodeling of their
                      mitochondrial network: while astrocytes within the penumbra
                      of the lesion undergo mitochondrial elongation, those
                      located in the core-the area invaded by proinflammatory
                      cells-experience transient mitochondrial fragmentation. In
                      brain slices, proinflammatory stimuli reproduced localized
                      changes in mitochondrial dynamics, favoring fission over
                      fusion. This effect was triggered by Drp1 phosphorylation
                      and ultimately resulted in reduced respiratory capacity.
                      Furthermore, maintenance of the mitochondrial architecture
                      critically depended on the induction of autophagy. Deletion
                      of Atg7, required for autophagosome formation, prevented the
                      reestablishment of tubular mitochondria, leading to marked
                      reactive oxygen species accumulation and cell death. Thus,
                      our data reveal autophagy to be essential for regenerating
                      astrocyte mitochondrial networks during inflammation.},
      keywords     = {Animals / Astrocytes: cytology / Astrocytes: drug effects /
                      Astrocytes: metabolism / Autophagy / Autophagy-Related
                      Protein 7 / Cells, Cultured / Cytokines: metabolism /
                      Dynamins: metabolism / Inflammation: metabolism /
                      Inflammation: pathology / Interferon-gamma: pharmacology /
                      Interleukin-1beta: metabolism / Lipopolysaccharides:
                      toxicity / Male / Mice / Mice, Inbred C57BL / Mice,
                      Transgenic / Microtubule-Associated Proteins: genetics /
                      Microtubule-Associated Proteins: metabolism / Mitochondria:
                      drug effects / Mitochondria: metabolism / Mitochondrial
                      Dynamics: drug effects / Nitric Oxide Synthase Type II:
                      metabolism / Phosphorylation / Reactive Oxygen Species:
                      metabolism / Atg7 protein, mouse (NLM Chemicals) / Cytokines
                      (NLM Chemicals) / Interleukin-1beta (NLM Chemicals) /
                      Lipopolysaccharides (NLM Chemicals) / Microtubule-Associated
                      Proteins (NLM Chemicals) / Reactive Oxygen Species (NLM
                      Chemicals) / Interferon-gamma (NLM Chemicals) / Nitric Oxide
                      Synthase Type II (NLM Chemicals) / Dnm1l protein, mouse (NLM
                      Chemicals) / Dynamins (NLM Chemicals) / Autophagy-Related
                      Protein 7 (NLM Chemicals)},
      cin          = {München Pre 2020},
      ddc          = {570},
      cid          = {I:(DE-2719)6000016},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24315370},
      doi          = {10.1016/j.cmet.2013.11.005},
      url          = {https://pub.dzne.de/record/137156},
}