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Tendon injuries initially suffer from: Poor blood supply Limited vascularity Slow nutrient delivery In rodent models, BPC-157 appears to: Upregulate VEGFR2 signalling Increase capillary density Improve microvascular perfusion Mechanistically: BPC-157 → VEGFR2 activation → PI3K/Akt pathway → eNOS phosphorylation → Increased nitric oxide → Improved angiogenesis More vascularity = better nutrient and oxygen delivery to fibroblasts
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Nonetheless, experiments using antioxidant compounds have generally been performed in short-lived species so that experiments can be completed in a feasible time frame
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