Hierarchical dual-conductive networks enable high-cell-density spheroid bioprinting for volumetric muscle loss repair.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Volumetric muscle loss (VML) remains a significant clinical challenge, as the intrinsic regenerative capacity of skeletal muscle is insufficient for restoring large tissue defects, often leading to extensive fibrotic scarring. While 3D bioprinting enables precise control over tissue architecture, challenges remain in high-cell-density printing and in maintaining cell viability during extrusion and photocrosslinking. Herein, we report a dual-conductive, cell spheroid-laden, bioprinted hydrogel construct for in situ VML repair. Specifically, myogenically differentiated adipose-derived stem cells (M-ADSCs) were assembled with carbon nanotube-loaded short fibers (F C ) into cell spheroids (F C -CS). These spheroids were then encapsulated within a hydrogel matrix containing additional F C , yielding the final F C -CS@Gel-F C . This spheroid-based printing strategy effectively shields M-ADSCs from nozzle-induced shear stress during high-cell-density bioprinting, while the integrated F C establishes a dual-conductive network. This network functions as an internal micro-scaffold within spheroids while forming conductive bridges between them in hydrogels, thereby enhancing electrical signal transmission, promoting cytoskeletal proteins expression, and facilitating myotube fusion. In vivo evaluation in a VML rat model demonstrates that F C -CS@Gel-F C significantly suppresses fibrotic sc

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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