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

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. To investigate the transcriptional changes in human primary chondrocytes upon silencing of the TL1A gene, human primary chondrocytes were divided into two groups: the control group (siNC), transfected with non-targeting siRNA, and the experimental group (siTL1A), transfected with siRNA targeting TL1A, each with three biological replicates (siNC1, siNC2, siNC3; siTL1A1, siTL1A2, siTL1A3). After 48-72 hours of transfection, total RNA was extracted, and its quality assessed before preparing RNA-Seq libraries. Transcriptome sequencing was performed on the Illumina NovaSeq 6000 platform to identify differentially expressed genes (DEGs) between the siNC and siTL1A groups.