Spinal cystic echinococcosis represents a severe therapeutic challenge in endemic regions, characterized by progressive osseous destruction and high rates of recurrence following surgical intervention. The pathogenic mechanisms underpinning parasitic establishment and survival, particularly the role of host-derived angiogenesis, remain poorly elucidated, hindering the development of targeted therapies. This study identifies a critical host signaling axis, involving the transcription factor Nrf2 and its downstream target RTN4, which is exploited by Echinococcus granulosus to stimulate neovascularization. Elucidating this Nrf2/RTN4 regulatory pathway provides fundamental insights into host-parasite interactions and unveils a novel mechanistic basis for angiogenesis within the unique bony microenvironment. These findings position the Nrf2/RTN4 axis as a promising therapeutic target for anti-angiogenic strategies aimed at improving the management of this debilitating disease.
Huang et al. (2026) studied this question.