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TDP43 augments astrocyte inflammatory activity through mtDNA-cGAS-STING axis in NMOSD.

Zhuhe Liu1, Yunmeng Bai2, Bingtian Xu3

  • 1Department of Neurology, Center for Medical Research on Innovation and Translation, Institute of Clinical Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.

Journal of Neuroinflammation
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Summary

Transactivating response region DNA binding protein 43 (TDP43) upregulation exacerbates neuromyelitis optica spectrum disorder (NMOSD) by activating astrocyte inflammation via the mitochondrial DNA/cyclic GMP-AMP synthase/stimulator of interferon genes pathway. Targeting TDP43 offers a potential therapeutic strategy for NMOSD.

Keywords:
Inflammatory activationMitochondrial dysfunctionNMOSDTDP43cGAS/STING

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Area of Science:

  • Neuroimmunology
  • Molecular Neuroscience
  • Cellular Pathology

Background:

  • Abnormal transactivating response region DNA binding protein 43 (TDP43) is a hallmark of neurodegenerative diseases.
  • The role of TDP43 in neuromyelitis optica spectrum disorder (NMOSD) is currently unknown.

Purpose of the Study:

  • To investigate the role and mechanism of TDP43 in NMOSD pathogenesis.
  • To explore TDP43 as a potential therapeutic target for NMOSD.

Main Methods:

  • Utilized in vitro and in vivo NMOSD models, patient samples, and single-nucleus RNA sequencing.
  • Examined TDP43 translocation, mitochondrial dysfunction, and the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway.
  • Assessed the effects of TDP43 knockdown/overexpression and cGAS/STING inhibitors on NMOSD-induced injury.

Main Results:

  • TDP43 was upregulated in NMOSD models and patients, associated with A1-like reactive astrocytes and mitochondrial dysfunction.
  • NMOSD induced TDP43 translocation to mitochondria, releasing mitochondrial DNA (mtDNA) and activating the mtDNA/cGAS/STING pathway.
  • TDP43 knockdown ameliorated NMOSD pathology, while overexpression exacerbated it; cGAS/STING inhibition also reduced NMOSD injury.

Conclusions:

  • TDP43 exacerbates astrocyte inflammation in NMOSD by upregulating the mtDNA/cGAS/STING signaling pathway.
  • Targeting TDP43 presents a promising therapeutic strategy for NMOSD treatment.