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The research team identified that erastin could directly bind to VDAC2/3, leading to loss of mitochondrial function as well as the emission of substantial amounts of oxides, finally causing ferroptosis (Yagoda et al., 2007)

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While it has not been conclusively established whether this dysfunction is a cause or consequence of the pathological processes, growing evidence suggests that reduced proteasomal activity may contribute to the accumulation of toxic protein aggregates and the progression of neurodegeneration