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[DOI] [PMC free article] [PubMed] [Google Scholar] Pawar S

Taken together, the convergence of ferritinophagy-derived labile iron and pathology-related mitophagy deficiency creates a hypersensitive state, heightening the induction of cell death by Erastin in EESCs

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Although alterations in genetic factors have been linked with its etiology, exponential accumulation of environmental entities such as reactive oxygen species (ROS) initiate a cyclic chain reaction resulting in accumulation of cellular inclusions, dysfunctional mitochondria, and overwhelming of antioxidant machinery, thus accelerating disease pathogenesis

Current evidence suggests that FRDA pathogenesis creates a highly conducive environment for lipid peroxidation (Figure 1), driven by dysregulated iron handling, amino acid metabolic shifts, and the failure of both glutathione (GSH)-dependent and independent pathways [29,63]