P-15 promotes chondrocyte proliferation in osteoarthritis by regulating SFPQ to target the Akt-RUNX2 axis

Abstract

Osteoarthritis (OA) is a chronic joint disease characterized by degenerative articular cartilage changes and secondary hyperosteogeny [1], affecting 10–15% of adults over the age of 60 worldwide [2]. OA is a major cause of disability, and its incidence, which is related to sex, age, obesity, joint trauma, and other factors, is on the rise, bringing a huge economic burden to patients and society [3, 4]. The pathogenesis of OA involves a redox state imbalance leading to oxidative stress, aging, and apoptosis in chondrocytes, as well as decreased anabolism and increased catabolism of the extracellular matrix [5, 6]. After articular cartilage injury, it is mainly repaired by the proliferation and differentiation of chondrocytes. However, the proliferative capacity of chondrocytes is limited, and the quality and quantity of chondrocytes directly affect the repair [7]. Therefore, regulating chondrocyte proliferation and elucidating its molecular mechanism are of great significance for developing effective therapeutic strategies.