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Collectively, these observations establish that NRF2 alone can sustain sufficient transcriptional output to maintain cancer cell line growth and that metabolic reprogramming of cells driven by NRF2 does not require redox buffering via enhanced glutathione production

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Pathogens 12 (11), 1354

Zhao, M., et al., Activation of hepatic CREBH and Insig signaling in the anti-hypertriglyceridemic mechanism of R--lipoic acid

Therefore, the introduction of nanoparticles with GSH-responsive or -depleted characteristics can effectively sensitize radiotherapy and further significantly improve the anticancer therapeutic effect