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Redox-fibrosis: Impact of TGF Beta 1 on ROS Generators, Mediators and Functional Consequences

Cell 14, 926939

Therefore, early intervention in replenishing mGSH stores by supplying GSH precursor such as N -acetylcysteine (NAC) or targeting upstream mechanisms involved in mitochondrial dysfunction and ROS generation, such as the sustained activation of c-Jun N-terminal kinases (JNK), can result in the protection of APAP-mediated hepatotoxicity