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As a result of hypoxic insults, the hypoxia-inducible factor 1α (HIF-1α), a potent cytokine, triggers downstream transductions that activate glial cells, leading to neuroinflammation, similar to the events observed in glaucoma associated with a high IOP [14,80,81]

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But native TGF-β is unstable, costly, and prone to side effects, and it loses its protective punch in aging cartilage as signaling drifts toward the SMAD1/5/8 route linked to hypertrophy.17 The elegant workaround: short synthetic peptides — cytomodulins (typically 4–6 amino acids, such as CM-10) and TGF-β1-derived sequences like YYVGRKPK — that mimic the signal with greater stability, lower immunogenicity, and lower cost.17,18 The regeneration frontier: growth-factor-mimicking peptides anchored to a scaffold coax stem cells into new cartilage