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Activation of a metabolic gene regulatory network downstream of mTOR complex 1

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doi:10.1016/B978-0-323-54391-0.00011-4

Furthermore, ALA attenuated MI by inducing M2b macrophage polarization through HMGB1/NF-B-pathway-mediated inflammation, oxidative stress, autophagy, and apoptosis, providing a hopeful strategy for the treatment of MI (Figure 5A,B) [53]

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Variability in NFE2L2 and KEAP1 mutations, coupled with nongenetic mechanisms such as p62/SQSTM1 accumulation, results in highly variable NRF2 activity across tumors, complicating the unification of therapeutic approaches [5, 56]