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At the molecular level, BPC-157 activates VEGFR2 signaling to drive new vessel formation at wound sites, mobilizes FAK-paxillin complexes that govern cell adhesion and directional migration, and upregulates growth hormone receptor expression in fibroblasts dramatically amplifying the healing cascade

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By comparison, the experimental groups from all three nerve injury models showed an improvement in nerve regeneration evidenced by CMAP amplitude and histomorphometry, although not all studies achieved statistical significance

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