In the present study, 24 rabbits were firstly used to evaluate the apoptosis index and matrix degeneration after untreated adult meniscal tears. Vertical tears (0.25 cm in length) were prepared in the avascular zone of the anterior horn. Specimens were harvested at 1, 3, 6, 12 weeks postoperatively. The apoptosis index around tear sites stayed at a high level throughout the whole follow-up period. The depletion of glycosaminoglycans (GAG) and aggrecan at the tear site was observed, while the deposition of COL I and COL II was not affected, even at the last follow-up of 12 weeks after operation. The expression of SOX9 decreased significantly; no cellularity was observed at the wound interface at all timepoints. Secondly, another 20 rabbits were included to evaluate the effects of anti-apoptosis therapy on rescuing meniscal cells and enhancing meniscus repair. Longitudinal vertical tears (0.5 cm in length) were made in the meniscal avascular body. Tears were repaired by the inside-out suture technique, or repaired with sutures in addition to fibrin gel and blank silica nanoparticles, or silica nanoparticles encapsulating apoptosis inhibitors (z-vad-fmk). Samples were harvested at 12 months postoperatively. We found the locally administered z-vad-fmk agent at the wound interface significantly alleviated meniscal cell apoptosis and matrix degradation, and enhanced meniscal repair in the avascular zone at 12 months after operation. Thus, local administration of caspase inhibitors (z-vad-fmk) is a promising therapeutic strategy for alleviating meniscal cell loss and enhancing meniscal repair after adult meniscal tears in the avascular zone.

Background: Visual impairment frequently impairs balance and motor coordination, yet the underlying neural circuit mechanisms remain poorly understood and require further investigation. In this study, we established a mouse model of visual impairment to assess the effects of defective vision on balance and coordination and further elucidated the functional role of the V1-M2 neural circuit in this process. Methods: A mouse model of corneal alkali burn was generated. Corneal morphology was observed, visual function was detected, and balance as well as motor coordination were evaluated. Neuronal activation in the V1 and M2 brain regions was quantified via c-Fos immunostaining. Viral tracing was performed to map the V1-M2 neural pathway, and chemogenetic manipulation was applied to modulate the V1-M2 circuit. Results: Mice subjected to corneal alkali burn exhibited abnormal corneal morphology and impaired visual function, accompanied by significant deficits in balance and motor coordination. The number of c-Fos⁺ neurons was markedly reduced in both the V1 and M2 regions. The direct V1-M2 neural circuit was anatomically verified. Chemogenetic activation of the V1-M2 circuit elevated c-Fos expression in M2 and rescued impaired motor performance. Conclusions: Visual impairment disrupts balance and motor coordination in mice. The V1 and M2 cortical areas mediate this behavioral dysfunction, likely due to attenuated activation of the V1-M2 neural circuit. These findings identify a promising neural circuit for dissecting the fundamental mechanisms underlying visuomotor integration.