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Closely related to oxidative stress is the so-called dicarbonyl stress, i.e., the accumulation of dicarbonyl metabolites leading to cell and tissue disfunction (40)
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Furthermore, mutations in the PINK1/Parkin pathway impair clearance of damaged mitochondria, allowing accumulated oxidized mitochondrial components to promote apoptosis via BAX binding or enhance ferroptosis susceptibility by activating ACSL4 [201]
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