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Chondrocytes are the sole cells found in the lacunae of the cartilage, a connective tissue with flexible property found in various regions of the mammalian bodies, including joints, nose and ear. They synthesise the collagen, proteoglycans and elastin fibres that make up the cartilage.
Increasing evidence suggested that dysregulation in lipid metabolism is linked to OA pathogenesis, but the underlying regulatory mechanism is not well understood. Here, the authors show that PPARα-ACOT12 signalling regulates cartilage homeostasis by regulating de novo lipogenesis in mice.
Osteoarthritis (OA) is associated with cartilage disruption, but the underlying mechanisms remain unclear. Here, the authors show that expression of osteoclast-associated receptor (OSCAR) is associated with OA, that its genetic ablation or targeting with OSCAR-Fc fusion protein ameliorates OA in mice by decreasing chondrocyte apoptosis.
Fibroblast growth factor signalling pathways have crucial roles in the development and maintenance of healthy cartilage. In this Review, the authors discuss strategies for targeting these pathways in osteoarthritis and cartilage repair.
Excessive mechanical stress promotes the development of osteoarthritis. Here Chang et al. identify gremlin-1 as a factor expressed in chondrocytes in response to mechanical stress, and contributing to osteoarthritis via activation of the NF-κB pathway.
Age-related stiffening of the extracellular matrix in cartilage promotes chondrocyte ageing in an epigenetically controlled process involving repression of the longevity protein α-Klotho.
A new study demonstrates that a single-cell mass cytometry approach can provide a precise snapshot of how candidate drugs affect chondrocyte subpopulations from patients with osteoarthritis.
