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doi: 10.1371/journal.pone.0179124 500 LoebelMStrohscheinKGianniniCKoelschUBauerSDoebisCet al
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The observation that BPC-157 appears to activate this pathway (via phosphorylation of FAK and paxillin) in cultured fibroblasts provides a direct molecular explanation for how it might accelerate wound closure and tissue repair in research models
The disorder might occur due to weakness or failure of the bone marrow
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Professor and Chair, Department of Nutritional Sciences Rutgers, The State University of New Jersey Copyright 2000-2026 Linus Pauling Institute Figure Alternative Text Figure 1
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