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Under pathological stimulation, overactivation of microglia leads to the release of large amounts of pro-inflammatory factors, ROS, and nitric oxide (NO), triggering uncontrolled inflammatory responses that ultimately result in neuronal damage and sustained neuroinflammation [68]

Such metabolic reprogramming enables T cells to swiftly adapt to diverse immune microenvironments, ensuring rapid and effective responses during inflammation (Fig

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Considerable genetic studies in SLE patients and animal models implicate the role of oxidative stress in the pathogenesis of SLE

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NAC treatment modulates the integrins 51 and PI3K/AKT signaling in TSPCs We further validated whether NAC treatment modulated the integrin 51 and PI3K/AKT signaling in TSPCs by immunofluorescence