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

GSE286153 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/02/01 Platform GPL24676
Summary
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.
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Also filed as BioProject PRJNA1208006 and SRA study SRP556069. Searching any of these in the dataset finder brings you back here.

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