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Specifically, the ROS scavenger butylated hydroxyanisole delayed TNF-induced necroptosis but had no effect on necroptosis induced by direct RIPK3 oligomerization, suggesting that ROS may facilitate upstream signaling events rather than serve as an obligate execution mechanism 80

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The combined administration of CsA and Fer-1 substantially alleviated corneal injury and DED marker upregulation, and CF@SNPs provide a promising solution to corneal injury in DED through the disruption of the inflammatory cascade, the generation of ROS, and ferroptosis

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