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Ferroptosis is a distinct, regulated form of cell death characterized by iron dependency and the accumulation of lipid peroxides, leading to oxidative damage and plasma membrane rupture. It is primarily driven by dysregulated iron metabolism and reactive oxygen species (ROS) generation, resulting in lethal lipid peroxidation. Key components include iron metabolism, lipid peroxidation (PUFA-PLs, ACSL4, LOX), and antioxidant defense (GPX4, System Xc-, FSP1-CoQ10-NAD(P)H pathway). Regulation involves iron, amino acid, and lipid metabolism pathways, as well as ferritinophagy and NRF2 signaling. Ferroptosis has been implicated in various diseases associated with oxidative stress and disrupted iron homeostasis.
Various, including inhibition of System Xc-, inhibition of GPX4, iron chelation, and lipid peroxidation inhibition.
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