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In conclusion, a lack of hyperoxidation sensitivity, which means that a peroxiredoxin remains active under acute H 2 O 2 stress, leads to increased cell death probably due to oxidation of matrix glutathione (Fig 6B)

The study underscores the crucial role of TB-500 in facilitating cardiac recovery in conditions of oxygen deprivation, emphasizing its potential as a therapeutic agent for cardiac-related conditions [11]

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The residue of position 24 further away can interact polarly with the receptor and is probably beneficial in locating the hydrophobic region