In response to the commentary by Qi et al. (2025) on our recent study of α9 integrin in spinal cord repair, we provide clarifications on several factual and interpretative points. The α9 integrin binding site resides within the third fibronectin type III-like repeat of tenascin-C, which is not alternatively spliced, ensuring consistent ligand engagement. Multiple studies, including those by Dobbertin et al., Cimpean et al., and Tan et al. support the pro-regenerative role of α9 integrin and its ability to overcome CSPG-mediated inhibition through Src and FAK signalling. We further note that long-term studies are indeed warranted and have facilitated such research by depositing all constructs on Addgene. Contrary to the commentary’s claim, our study employed a spinal cord injury model, not a dorsal root crush, and histological data confirm the presence of a fibrotic scar. No evidence of neuropathic pain was observed at 12 weeks, indicating functional safety within the study timeframe. Together, these clarifications reaffirm that α9 integrin signalling directly promotes axon regeneration and that future work using temporally controlled systems will build on these findings.

Department of Clinical Neurosciences John Van Geest Centre for Brain Repair University of Cambridge Cambridge CB2 0PY UK

Faculty of Biological Sciences University of Leeds Leeds LS2 9JT UK

Institute of Experimental Medicine Czech Academy of Science Videnska 1083 Prague 4 14200 Prague Czech Republic

Zobrazit více v PubMed

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