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Enhanced secretory load, imbalances in redox homeostasis, or perturbations in protein homeostasis triggered by lysosomal or autophagosomal dysfunction may all cause ER stress and trigger the unfolded protein response (UPR)

Growing evidence underscores a complex crosstalk between ferroptosis and other key cellular processes, including metabolic reprogramming, autophagy, and immune regulation, all of which collectively shape ferroptosis susceptibility

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FIGURE 2 After the discovery of PKC, animal models used for the study of memory were applied to Ca++-dependent pkc