These findings suggest that EDIL3 functions as an important mediator of pathological vascular permeability and angiogenesis in the subchondral bone during OA progression. Targeting EDIL3 to restore subchondral bone microenvironment homeostasis may represent a novel therapeutic strategy for OA management.
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Ye Ma
Ke Feng
Kuanmin Tian
International Immunopharmacology
Ningxia Medical University
Ningxia Medical University General Hospital
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Ma et al. (Mon,) studied this question.
www.synapsesocial.com/papers/69df2b85e4eeef8a2a6b089f — DOI: https://doi.org/10.1016/j.intimp.2026.116637