Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis.

摘要: Osteoarthritis (OA) is a joint pathology characterized by progressive cartilage degradation. Medical care mainly based on alleviating pain symptoms. Compelling studies report the presence of empty lacunae and hypocellularity in with aging OA progression, suggesting that chondrocyte cell death occurs participates to development. However, relative contribution apoptosis per se pathogenesis appears complex evaluate. Indeed, depending technical approaches, stages, layers, animal models, as well vivo or vitro experiments, percentage types can vary. Apoptosis, chondroptosis, necrosis, autophagic are described this review. The question causality progression also addressed, molecular pathways leading response following inducers: Fas, Interleukin-1β (IL-1β), Tumor Necrosis factor-α (TNF-α), leptin, nitric oxide (NO) donors, mechanical stresses. Furthermore, protective role autophagy chondrocytes highlighted, its decline during enhancing death; transition being controlled HIF-1α/HIF-2α imbalance. Finally, we have considered whether interfering promoting could constitute therapeutic strategies impede progression.