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While the interplay between mitochondrial dysfunction and ferroptosis in diabetic ulcers is still unclear, targeting ferroptosis-related pathways holds significant therapeutic promise

In the context of cancer, ferroptosis may act as an endogenous tumor suppressive mechanism downstream of p53 [11]
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Long-term deficiency can lead to cognitive problems

Dysregulation of copper homeostasis interferes with the PARKIN/PINK1 pathway through multi-layered mechanisms (125)
