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Mutations in THAP11 cause an inborn error of cobalamin metabolism and developmental abnormalities

They: Produce collagen Organize extracellular matrix Restore tensile structure In experimental tendon transection models, BPC-157 has been associated with: Increased fibroblast density Enhanced migration into injury site Accelerated granulation tissue formation Proposed signalling involvement includes: FAK (Focal Adhesion Kinase) activation ERK1/2 signalling Src pathway modulation FAK signalling is particularly important because it regulates: Cell adhesion Cytoskeletal reorganization Migration along collagen scaffolds Tendon strength depends not just on collagen quantity but alignment