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More general longevity peptide than specific repair application

ROS are widely accepted as a source of oxidative stress that appears to be responsible for the initiation of necroinflammation

The two mechanisms are complementary rather than redundant and BPC-157s growth factor receptor upregulation and cytoprotective signalling creating a cellular environment permissive to repair, while TB-500s actin dynamics modulation and PI3K/Akt activation drive the cell migration, vascular ingrowth, and matrix remodelling that execute the repair process at the tissue level

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