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In TM cells, after exogenous oxidative treatment, the following damage has been observed: a decrease in cellular activity (102), a change in cell cycle progression, the inhibition of cell proliferation (103), and the promotion of cellular senescence (100)

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However, an emerging conceptual shift suggests that lipid peroxidation and ferroptosis significantly contribute to FRDA pathogenesis, acting in concert with other well-established disease mechanisms such as mitochondrial bioenergetic failure, apoptosis, and inflammatory signaling [29,30]