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Increased oxidative stress leads to the modification of redox-sensitive cysteine residues in Keap1, resulting in the release of Nrf2 and its translocation to the cell nucleus [75]

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[SOURCED] The angiogenic mechanism is closely linked to BPC-157s NO system effects: VEGF-driven angiogenesis is NO-dependent, and the compounds capacity to sustain eNOS activity under stress conditions may create favorable conditions for new vessel formation in ischemic tissue

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The gamma-glutamyl cycle should be considered not as a mechanism for amino acid transport but rather a generator of extracellular signals, gamma-glutamyl amino acids, that are converted intracellularly to 5-oxoproline, which activates uptake and/or metabolism of amino acids (1, 74, 75)