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Under stress conditions, mitochondrial damage results in the production of excessive mtROS, provoking oxidative damage to mtDNA and mtDNA release into the cytoplasm through the mitochondrial permeability transition pore, which further activates the DNA sensor cGAS-STING and facilitates downstream inflammatory processes (101, 102)
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Ablating microglia also reduces the number of functional synapses in juvenile mice (Miyamoto et al
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