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From there, it is transported via Transcobalamin II to body tissues

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16 Transfer of these vesicles to previously untreated recipient tubular cells induces a canonical ferroptotic phenotype, including loss of GPX4, accumulation of lipid ROS, increased malondialdehyde levels, and progressive membrane damage

This phenomenon results in the polarization of macrophages toward a pro-inflammatory M1 phenotype, thereby exacerbating the inflammatory response

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