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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Ma et al. (Mon,) studied this question.
synapsesocial.com/papers/69df2b85e4eeef8a2a6b089f — DOI: https://doi.org/10.1016/j.intimp.2026.116637
Ye Ma
Xinjiang Institute of Materia Medica
Ke Feng
Qingdao University of Science and Technology
Kuanmin Tian
Ningxia Medical University
International Immunopharmacology
Ningxia Medical University
Ningxia Medical University General Hospital
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