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Figure 4. EMs derived from SHED are directly incorporated into a polydopamine-modified GelMA (GM@PDA) hydrogel network. This direct incorporation strategy ensures localized and sustained delivery of EMs at the tendon-bone interface. The released EMs modulate macrophage polarization toward the regenerative M2 phenotype via autophagy activation, suppress NF-κB-mediated inflammation, and concurrently enhance the tenogenic and chondrogenic differentiation of stem cells, thereby accelerating integrated repair. Reprint with permission from Elsevier^[108]. EMs: Exosome-mimetics; SHED: stem cells from human exfoliated deciduous teeth; GelMA: gelatin methacryloyl; GM@PDA: GelMA hydrogel modified with polydopamine; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells.