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A key pathological mechanism implicated in SCI and DCM is neuroinflammation driven by prolonged activation of microglia and macrophages (M/M) in the central nervous system (Watanabe et al., 2015

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Under the influence of SLE serum or IFN-, neutrophils derived from healthy controls showed stronger binding of CREM to the GPX4 promoter and more nuclear accumulation, leading to GPX4 suppression and elevated lipid peroxidation (118)

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