A previous cellular study has found that treatment of chondrocytes isolated from femoral condyles of patients with OA with TGF-1, a cartilage protective factor and an important regulator of cartilage homeostasis, increased the expression of HK2 and glucose transporter 1(one of the key regulators of glycolysis), thereby stimulating enhanced aerobic glycolysis and increasing the production of abnormal metabolites (78)
This mechanism explains the peptides remarkable effects across tendons, ligaments, muscle tissue, gastrointestinal conditions, and nerve damage documented in 35 preclinical studies spanning three decades
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