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In vitro, oxidative stress activates apoptosis signal-regulating kinase 1 (ASK1), triggering downstream effectors, including JNK1/2 and p38MAPK

Richardson NE, Konon EN, Schuster HS, Mitchell AT, Boyle C, Rodgers AC, et al

The observation that restoration of the redox environment recovers ATP production and Complex I activity indicates the possibility that pharmacological agents can be designed and targeted to mitochondria to ameliorate deregulated S-glutathionylation reactions