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A simplified view of the proposed cascade looks like this: VEGFR2 activation triggers downstream signaling through the Akt-eNOS axis eNOS activation increases local nitric oxide availability, supporting vessel relaxation and perfusion FAK-paxillin signaling enables endothelial cells to migrate and form new vascular structures In tendon tissue specifically, growth hormone receptor upregulation runs in parallel, increasing cell sensitivity to circulating growth hormone Reduced inflammatory cytokine activity and improved fibroblast function support the broader tissue environment needed for repair to proceed A 2025 scoping review summarizing 36 studies — 35 preclinical and one clinical — concluded that BPC-157 activates several overlapping pathways, notably VEGFR2 and nitric oxide synthesis via the Akt-eNOS axis, promoting angiogenesis, fibroblast activity, and neuromuscular stabilization in musculoskeletal healing models (Vasireddi et al., Orthopaedic Journal of Sports Medicine 2025)
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