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Excess NEFAs, which stimulate the secretion of insulin, disrupt the function of cells by increasing basal insulin levels but inhibit GSIS

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The accumulation of A within neuron cells also disrupted the activity of the ubiquitin-proteasome [167, 168]

Figure 10 7 Limitations and future directions of ferroptosis in neurodegenerative diseases Although mounting evidence highlights the critical role of ferroptosis in the onset and progression of neurodegenerative diseases, and its status as a novel mode of cell death is increasingly recognized, the field remains at an early stage of conceptual integration and mechanistic exploration