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Animal experiments show that the use of iron chelators or GPX4 activators can not only reduce ferroptosis markers but also decrease TUNEL-positive apoptotic cells and the extent of alveolar structural damage (207), indicating that by alleviating iron overload and lipid peroxidation, the death mode selection can be redirected from highly lytic, pro-inflammatory ferroptosis back to a relatively silent apoptotic phenotype, thereby reducing DAMPs release and subsequent inflammatory amplification (208)

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