ArticlebioRxiv : the preprint server for biology2025
Complement factor D (adipsin) mediates pressure-pain hypersensitivity post destabilization of medial meniscus injury.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAlthough osteoarthritis (OA) is the leading cause of pain and disability worldwide, there is a lack of models to probe the separable mechanism of OA structural damage and knee pain. We previously identified that deletion of complement factor D (FD) results in increased pressure-pain hyperalgesia despite cartilage protection after destabilization of the medial meniscus (DMM) surgery. However, how these discordant OA phenotypes manifest is not understood. We employed a novel targeted lipidomics approach to elucidate the role of eicosanoids in FD-mediated pain. We hypothesize that the absence of
methodsMale and female
resultsIn contrast to WT mice,
conclusionThe absence of
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