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For example, macrophage-derived Exos induce endothelial ferroptosis and barrier disruption during cerebral ischemiareperfusion injury via thrombospondin-1-mediated binding to OTUD5 and promotion of GPX4 ubiquitination [221]

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Redox signaling modulates their functions, impacting processes such as antigen presentation, microbial killing, cytotoxic activity, and maintenance of gut homeostasis

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