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A key pathway involves the activation of the FAK-paxillin signaling cascade

This FAK-paxillin signaling axis connects BPC-157's molecular pharmacology to its observed tissue-level effects in a mechanistically coherent way: a compound that enhances endothelial FAK activation will simultaneously promote cell survival (resistance to anoikis), cell migration (capillary sprouting), and cell-matrix adhesion (structural integrity of new vessels)

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