WP5373 - Osteoarthritic chondrocyte hypertrophy - Homo sapiens

Hypoxia in osteoarthritis (OA) leads to low oxygen levels in cartilage, activating hypoxia-inducible factors (HIFs). Angiogenesis occurs in response to hypoxia, stimulating the formation of new blood vessels. Vascular endothelial growth factor (VEGF) plays a key role in angiogenesis. Dysregulation of the canonical FGF signalling pathway disrupts chondrocyte proliferation and differentiation. In OA, aberrant FGF signalling contributes to the hypertrophic chondrocyte phenotype. This phenotype is associated with increased cell size, altered gene expression and matrix degradation. Understanding these interactions may provide therapeutic insights for the treatment of OA.
The pathway is based on Figure 5 of the paper by Ellen G. J. Ripmeester et al. (2018).