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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)

Because bladder tissues cannot easily be collected in clinical trials, animal investigations have been conducted to study the molecular mechanism of SUI

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4a, b), while LPCAT3 is increased significantly about 2-fold between 7 and 35 days after SCI (Fig