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In cardiomyocytes, ROS activate ERK/p38 MAPK pathways to mediate hypertrophy and induce apoptosis via JNK/p53 pathways and mitochondrial membrane permeability alterations [323, 324]

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Condensation of the cell membrane without affecting membrane integrity, blistering of the plasma membrane, increased density of the mitochondrial membrane, reduction or disappearance of the mitochondrial crest, and rupture of the mitochondrial outer membrane are typical characteristics of ferroptosis (Figure 1) ( in vivo

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