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In the hypertensive kidney, mitochondrial dysfunction can result in excess production of mitochondrial reactive oxygen species (mtROS), which activate redox-sensitive transcription factors like NF-B, activator protein 1 (AP-1), and others that drive the expression of pro-inflammatory cytokines (e.g., TNF-, IL-6, and IL-1), contributing to a microenvironment that favors renal injury

Your body produces it on its own, but production declines significantly with age, from roughly 200 ng/mL at age 20 to around 80 ng/mL by age 60

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[DOI] [PMC free article] [PubMed] [Google Scholar] 60.Andreasson A., Hagstrm H., Skldberg F., nnerhag K., Carlsson A.C., Schmidt P.T., Forsberg A.M

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This potentially suggests that BPC-157 may activate the FAK-paxillin pathway, which may be involved in the promotion of tendon fibroblast migration and cell adhesion