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Oxidative stress in FRDA patients is thought to result from the production of reactive oxygen species catalyzed by free iron accumulating in mitochondria (Fenton reaction) and from impaired oxidative stress signaling by the master regulator NRF2 (NF-E2-related factor) allowing reactive oxygen species to accumulate (Pastore and Puccio, 2013)
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GHK-Cu was also studied in connection with wound-related extracellular matrix formation
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