Osteoarthritis pathogenesis is driven by IgE-mediated mast cell activation.

Low expression of Cbfb may be the cause of osteoarthritis, and local admission of Cbfb may rescue and protect against osteoarthritis through decreasing Wnt/β-catenin signaling, and increasing Hippo/Yap signaling and Tgfβ/Smad2/3 signaling in osteoarthritis articular cartilage.

Parathyroid hormone attenuates osteoarthritis pain and joint degeneration by modification of subchondral bone remodeling and could be a potential disease-modifying therapy for osteoarthritis.

Under metabolic syndrome, joint subchondral preosteoclasts acquire a senescence-associated secretome, which causes a rapid structural alteration of subchondral bone and contributes to the development of osteoarthritis.

Down-regulation of GAS6 by M1 macrophages resulted in impaired efferocytosis for synovial apoptotic cells, causing synovial hyperplasia and obesity-associated OA development.

Serum exosomal sequencing combined with cell and animal experiments indicate that miRNA-199b-5p is a novel miRNA associated with osteoarthritis (OA) and can modulate the onset and progression of the disease.

Osteoblastic PGE2 induces pain and OA progression by Na_V1.8 modification and serves as a potential target multiple skeletal pain and degenerations.

Protein dynamics signatures in ageing collagen-rich tissues that are central to frequent age-related diseases such as osteoporosis and osteoarthritis.

Corefucosylation contributes to the maintenance of the articular cartilage phenotype and depletion of FUT8 inhibits recovery from cartilage damage and promotes cartilage degeneration.

Disruption of the intracellular vimentin network upon cellular stress results in enhanced cell surface vimentin on human osteoarthritic chondrocytes and might represent a novel membrane-associated marker of stress-induced premature senescence.