作者
Elisa Motori, Julien Puyal, Nicolas Toni, Alexander Ghanem, Cristina Angeloni, Marco Malaguti, Giorgio Cantelli-Forti, Benedikt Berninger, Karl-Klaus Conzelmann, Magdalena Götz, Konstanze F Winklhofer, Silvana Hrelia, Matteo Bergami
发表日期
2013/12/3
期刊
Cell metabolism
卷号
18
期号
6
页码范围
844-859
出版商
Elsevier
简介
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 …
引用总数
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