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| 001 | 137156 | ||
| 005 | 20240321220212.0 | ||
| 024 | 7 | _ | |a 10.1016/j.cmet.2013.11.005 |2 doi |
| 024 | 7 | _ | |a pmid:24315370 |2 pmid |
| 024 | 7 | _ | |a 1550-4131 |2 ISSN |
| 024 | 7 | _ | |a 1932-7420 |2 ISSN |
| 024 | 7 | _ | |a altmetric:1967201 |2 altmetric |
| 037 | _ | _ | |a DZNE-2020-03478 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 570 |
| 100 | 1 | _ | |a Motori, Elisa |0 P:(DE-HGF)0 |b 0 |e Corresponding author |
| 245 | _ | _ | |a Inflammation-induced alteration of astrocyte mitochondrial dynamics requires autophagy for mitochondrial network maintenance. |
| 260 | _ | _ | |a Cambridge, Mass. |c 2013 |b Cell Press |
| 264 | _ | 1 | |3 print |2 Crossref |b Elsevier BV |c 2013-12-01 |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1585560983_22216 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a 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. |
| 536 | _ | _ | |a 341 - Molecular Signaling (POF3-341) |0 G:(DE-HGF)POF3-341 |c POF3-341 |f POF III |x 0 |
| 542 | _ | _ | |i 2013-12-01 |2 Crossref |u https://www.elsevier.com/tdm/userlicense/1.0/ |
| 542 | _ | _ | |i 2014-12-03 |2 Crossref |u https://www.elsevier.com/open-access/userlicense/1.0/ |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 7 | |a Atg7 protein, mouse |2 NLM Chemicals |
| 650 | _ | 7 | |a Cytokines |2 NLM Chemicals |
| 650 | _ | 7 | |a Interleukin-1beta |2 NLM Chemicals |
| 650 | _ | 7 | |a Lipopolysaccharides |2 NLM Chemicals |
| 650 | _ | 7 | |a Microtubule-Associated Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Reactive Oxygen Species |2 NLM Chemicals |
| 650 | _ | 7 | |a Interferon-gamma |0 82115-62-6 |2 NLM Chemicals |
| 650 | _ | 7 | |a Nitric Oxide Synthase Type II |0 EC 1.14.13.39 |2 NLM Chemicals |
| 650 | _ | 7 | |a Dnm1l protein, mouse |0 EC 3.6.5.5 |2 NLM Chemicals |
| 650 | _ | 7 | |a Dynamins |0 EC 3.6.5.5 |2 NLM Chemicals |
| 650 | _ | 7 | |a Autophagy-Related Protein 7 |0 EC 6.2.1.45 |2 NLM Chemicals |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a Astrocytes: cytology |2 MeSH |
| 650 | _ | 2 | |a Astrocytes: drug effects |2 MeSH |
| 650 | _ | 2 | |a Astrocytes: metabolism |2 MeSH |
| 650 | _ | 2 | |a Autophagy |2 MeSH |
| 650 | _ | 2 | |a Autophagy-Related Protein 7 |2 MeSH |
| 650 | _ | 2 | |a Cells, Cultured |2 MeSH |
| 650 | _ | 2 | |a Cytokines: metabolism |2 MeSH |
| 650 | _ | 2 | |a Dynamins: metabolism |2 MeSH |
| 650 | _ | 2 | |a Inflammation: metabolism |2 MeSH |
| 650 | _ | 2 | |a Inflammation: pathology |2 MeSH |
| 650 | _ | 2 | |a Interferon-gamma: pharmacology |2 MeSH |
| 650 | _ | 2 | |a Interleukin-1beta: metabolism |2 MeSH |
| 650 | _ | 2 | |a Lipopolysaccharides: toxicity |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Mice, Inbred C57BL |2 MeSH |
| 650 | _ | 2 | |a Mice, Transgenic |2 MeSH |
| 650 | _ | 2 | |a Microtubule-Associated Proteins: genetics |2 MeSH |
| 650 | _ | 2 | |a Microtubule-Associated Proteins: metabolism |2 MeSH |
| 650 | _ | 2 | |a Mitochondria: drug effects |2 MeSH |
| 650 | _ | 2 | |a Mitochondria: metabolism |2 MeSH |
| 650 | _ | 2 | |a Mitochondrial Dynamics: drug effects |2 MeSH |
| 650 | _ | 2 | |a Nitric Oxide Synthase Type II: metabolism |2 MeSH |
| 650 | _ | 2 | |a Phosphorylation |2 MeSH |
| 650 | _ | 2 | |a Reactive Oxygen Species: metabolism |2 MeSH |
| 700 | 1 | _ | |a Puyal, Julien |0 P:(DE-HGF)0 |b 1 |
| 700 | 1 | _ | |a Toni, Nicolas |0 P:(DE-HGF)0 |b 2 |
| 700 | 1 | _ | |a Ghanem, Alexander |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Angeloni, Cristina |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Malaguti, Marco |0 P:(DE-HGF)0 |b 5 |
| 700 | 1 | _ | |a Cantelli-Forti, Giorgio |0 P:(DE-HGF)0 |b 6 |
| 700 | 1 | _ | |a Berninger, Benedikt |0 P:(DE-HGF)0 |b 7 |
| 700 | 1 | _ | |a Conzelmann, Karl-Klaus |0 P:(DE-HGF)0 |b 8 |
| 700 | 1 | _ | |a Götz, Magdalena |0 P:(DE-HGF)0 |b 9 |
| 700 | 1 | _ | |a Winklhofer, Konstanze F |0 P:(DE-2719)9000369 |b 10 |u dzne |
| 700 | 1 | _ | |a Hrelia, Silvana |0 P:(DE-HGF)0 |b 11 |
| 700 | 1 | _ | |a Bergami, Matteo |0 P:(DE-HGF)0 |b 12 |
| 773 | 1 | 8 | |a 10.1016/j.cmet.2013.11.005 |b : Elsevier BV, 2013-12-01 |n 6 |p 844-859 |3 journal-article |2 Crossref |t Cell Metabolism |v 18 |y 2013 |x 1550-4131 |
| 773 | _ | _ | |a 10.1016/j.cmet.2013.11.005 |g Vol. 18, no. 6, p. 844 - 859 |0 PERI:(DE-600)2174469-5 |n 6 |q 18:6<844 - 859 |p 844-859 |t Cell metabolism |v 18 |y 2013 |x 1550-4131 |
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| 910 | 1 | _ | |a Deutsches Zentrum für Neurodegenerative Erkrankungen |0 I:(DE-588)1065079516 |k DZNE |b 10 |6 P:(DE-2719)9000369 |
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