TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [II]

Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage degradation, chronic inflammation, and chondrocyte senescence. Tumor necrosis factor-like cytokine 1A (TL1A), a member of the TNF superfamily, has recently been implicated in regulating inflammatory processes and tissue remodeling. However, its precise role in OA pathogenesis remains incompletely understood. In this study, we investigated the impact of TL1A deficiency on OA progression and its underlying mechanism with a focus on oxidative stress-induced chondrocyte senescence. Clinical sample collection in this study was reviewed and approved by the Institutional Review Board (IRB) of the First Hospital of China Medical University (EC-2021-HS-004). All patients involved in this study gave informed consent. Paired smooth and damaged cartilage was obtained from the same OA patients undergoing total knee arthroplasty (n = 8). The difference between the smooth (relatively healthy area) and damaged (severely damaged area) articular surfaces was distinguished using the Mankin scoring system[33]. Detailed patients’ information is listed in Table S2.