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Our results suggest that the promotion of a ferroptosis-vulnerable stage induced by CDK4/6 and ER inhibitors, is dependent on cell cycle arrest, which leads to a redox-lipid imbalance with increased PUFA generation, reduced GPX4 and ferritin levels, and increased lipid peroxidation (Fig
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Insulin-resistant condition contributes to factor the decreased availability of NO in the endothelium, and it may be caused by reductions in the enzyme endothelial NOS, a lack of substrate or cofactors for endothelial NOS, and alterations in intracellular signaling [34]
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