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and acts via glutathione (GSH)-dependent mechanisms, with synergistic effects alongside reactive oxygen species (ROS) to exacerbate erythrocyte death Mechanistically, IS induces eryptosis through multiple interconnected pathways: it elevates intracellular Ca 2+ concentrations, triggering membrane phospholipid scrambling and subsequent phosphatidylserine (PS) externalization

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Whether this effect results in a net gain of pro- or anti-inflammatory lipids is controversial, because only some of these oxPL are highly potent inflammatory mediators, while others are partial agonists that might therefore antagonize inflammatory responses to other mediators like LPS

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