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The Nrf2-induced expression of heme oxygenase 1 inhibits the pro-inflammatory signaling operated by NFB [144], while free Keap1 following Nrf2 dissociation can additionally amplify this effect, through the production of adducts with IKK, which is a positive regulator of NFB [145]

BPC-157's angiogenic properties target exactly this bottleneck

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