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You cannot force cell turnover without disrupting the existing barrier
Causal attribution of specific gene-expression changes to GHK-Cu, and replication of those signatures in independent experimental systems, are the kind of follow-on work that would move the field from correlation toward mechanism
Published preclinical work has examined BPC-157 in rat tendon explants and cultured fibroblasts
This does not reduce the total amount of GHK-Cu delivered
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