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Mitochondrial DNA Leakage and cGas/STING Pathway in Microglia: Crosstalk Between Neuroinflammation and Neurodegeneration
Mitochondrial DNA Escape and Immune Response in Brain Support Cells: Links Between Brain Inflammation and Nerve Cell Damage
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Abstract
Chronic neuroinflammation is a hallmark of neurodegenerative diseases characterized by abnormal protein deposition and neuronal loss.
- Microglia, the brain's primary immune cells, play a key role in creating an inflammatory environment associated with neurodegeneration.
- Cytoplasmic free mitochondrial DNA (mtDNA) can activate the cGas/STING signaling pathway, leading to the production of type I interferon and proinflammatory cytokines.
- Mitochondrial oxidative stress is a major contributor to the accumulation of free mtDNA in microglial cells.
- Upregulation of the cGas/STING pathway in microglia is linked to persistent activation and increased release of neurotoxic inflammatory mediators like interleukin-6 and tumor necrosis factor-α.
- Excessive secretion of these inflammatory mediators may exacerbate neuronal damage and advance neurodegeneration.
- Targeting the regulation of the cGas/STING signaling pathway in microglia could offer a potential therapeutic strategy for slowing the progression of neurodegenerative disorders.
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