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. 2024 Jul 24;3(6):loae031.
doi: 10.1093/lifemeta/loae031. eCollection 2024 Dec.

Senescent glia-bridging neuronal mitochondrial dysfunction and lipid accumulation in aging

Affiliations

Senescent glia-bridging neuronal mitochondrial dysfunction and lipid accumulation in aging

Joel F Reyes et al. Life Metab. .
No abstract available

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Conflict of interest statement

The authors declare that no confict of interest exists.

Figures

Figure 1
Figure 1
In response to aging-induced mitochondrial dysfunction, neurons promote activator protein 1 (AP1)-driven senescence in glia. Intermittent blockade of AP1 signaling in glia reduces lipid droplet (LD) accumulation in non-senescent glia and extends healthspan. AP1+ glia promote LD accumulation in non-senescent glia through speculative secretory mechanisms. The figure was made using BioRender.

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