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Excess intracellular iron catalyzes Fenton reactions, generating reactive oxygen species (ROS) that oxidize polyunsaturated fatty acids (PUFAs) in membranes [88], resulting in membrane rupture and cell death (Fig

Pretreatment continued for 20 min before PE was added

Given that mitochondria are both a primary source of endogenous ROS and a central hub for iron metabolism, their membranes are uniquely vulnerable to ferroptotic insults

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How to maximally inhibit tumor growth without interfering with normal physiological activities is a key issue in the development of IGF-1/2 inhibitors