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The FAK-paxillin pathway, which regulates cell migration, adhesion, and survival, represents another key mechanism: BPC-157 activates this pathway in fibroblasts and endothelial cells, facilitating the cellular movement required for wound closure and structural tissue regeneration
This commonly occurred with all of the used BPC 157 therapeutic regimens as well as at both early and advanced stages (Vukojevic et al., 2018)