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From a formulation standpoint, this mechanism explains why we consistently observe greater stability in finished SAG products than in GSH: GSH oxidizes before it reaches the cell, whereas SAG arrives intact and activates on demand

Mechanistically, ferroptosis in transplanted hearts triggers the initial release of DAMPs, which bind to endothelial Toll-like receptor 4 (TLR4) and stimulate type I interferon production via Trif-mediated signaling, promoting the recruitment of neutrophils to the injured heart [103]

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