, collectively supporting reduced fibrosis and improved stability. Transcriptomic analysis revealed that BT activated the integrin-FAK/Src-MAPK signaling axis, driving tenogenic differentiation while suppressing fibrogenesis, thereby elucidating the molecular mechanism of enhanced tendon-prosthesis integration. Our results demonstrate that BT scaffolds effectively overcome fibrotic tendon-prosthesis interface healing and provide a promising strategy to address the long-standing challenge of insufficient interfacial mechanics in tendon-prosthesis reconstruction.
Zhang et al. (Wed,) studied this question.