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80 This body of evidence provides an additional link between oxidative stress and genetic factors in the pathogenesis of ASD

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Meanwhile, methyltransferase 3-mediated m6A modification promotes the degradation of synaptosomal-associated protein 29 mRNA, thereby impairing the restoration of autophagic flux, triggering mitochondrial crisis and excessive ROS accumulation, and ultimately exacerbating oxidative stress injury in the ischemic microenvironment (48)

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