Complement factor D (adipsin) mediates pressure-pain hypersensitivity post destabilization of medial meniscus injury.

ABSTRACT:

Background

Osteoarthritis (OA) is the leading cause of pain worldwide. However, clinical discordance between pain and cartilage damage presents challenges in determining the mechanisms of OA pain, thus creating a need for well-controlled models that probe the separable mechanisms of 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 Cfd (FD^-/-) will protect cartilage but cause i

SUBMITTER: Tjandra PM 

PROVIDER: S-EPMC12659361 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature