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performed and analyzed in vitro and in vivo experiments

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(170) demonstrated that treatment with the ferroptosis inducer (1S,3R)-RSL3 and the necroptosis inducer shikonin both triggered receptor-interacting protein kinase 3 (RIPK3) by lipid ROS accumulation and GPX4 inhibition, whereas necroptosis is accompanied by only a mild elevation of lipid ROS and is primarily marked by MLKL phosphorylation followed by translocation to the cell membrane, leading to increased membrane permeability