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The two mechanisms are complementary rather than redundant and BPC-157s growth factor receptor upregulation and cytoprotective signalling creating a cellular environment permissive to repair, while TB-500s actin dynamics modulation and PI3K/Akt activation drive the cell migration, vascular ingrowth, and matrix remodelling that execute the repair process at the tissue level

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Indirect evidence for this possibility was provided by the high expression levels of the SA-induced gene PR1 in untreated and BSO+GSH-treated sym33-3 plants relative to other genotypes (Figure 7)