ArticleBioengineered2022
Silence of TANK-binding kinase 1 (TBK1) regulates extracellular matrix degradation of chondrocyte in osteoarthritis by janus kinase (JAK)-signal transducer of activators of transcription (STAT) signaling.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 16 citations in OpenAlex.
- Activation of M1mAChR's improves spatial learning and memory deficits in rats exposed to chronic intermittent hypoxia.Scientific reports · 2026Article
- Therapeutic potential of IκB kinase epsilon inhibition in preventing meniscal degeneration of early osteoarthritis.Bone & joint research · 2025Article
- TBK1 pharmacological inhibition mitigates osteoarthritis through attenuating inflammation and cellular senescence in chondrocytes.Journal of orthopaedic translation · 2024Article
- Network pharmacology combined with experimental validation to investigate the effect of Rongjin Niantong Fang on chondrocyte apoptosis in knee osteoarthritis.Molecular medicine reports · 2024Article
- Human dental pulp stem cells derived extracellular matrix promotes mineralization via Hippo and Wnt pathways.Scientific reports · 2024Article
- cGAS-STING pathway in pathogenesis and treatment of osteoarthritis and rheumatoid arthritis.Frontiers in immunology · 2024Review
- The Role of Regulated Programmed Cell Death in Osteoarthritis: From Pathogenesis to Therapy.International journal of molecular sciences · 2023Review
- TBK1-medicated DRP1 phosphorylation orchestrates mitochondrial dynamics and autophagy activation in osteoarthritis.Acta pharmacologica Sinica · 2023Article
- The potential roles of JAK/STAT signaling in the progression of osteoarthritis.Frontiers in endocrinology · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
TANK-binding kinase 1 (TBK1) was previously reported to be critical for the regulation of osteoclast differentiation. However, its function in osteoarthritis (OA) has not yet been determined. This study aims to reveal the role of TBK1 in the extracellular matrix (ECM) degradation in OA. C57BL/6 J mice were subjected to anterior cruciate ligament transection (ACLT) surgery to establish an OA animal model. ATDC5 cells were treated with IL-1β to construct a cell model of OA. Changes in the expression of TBK1 were analyzed by qRT-PCR, Western blotting, and immunohistochemistry. Safranin O-fast green staining, ELISA, and Western blotting were performed to evaluate the ECM degradation. By searching GSE75181 and GSE6119 datasets, TBK1 was found to be highly expressed in the OA model. Its upregulation was also confirmed in ACLT mice and in a cell model of OA. Silencing of TBK1 reduced cartilage degradation, OARSI score, and serum levels of CTX-II and COMP. Silencing of TBK1 attenuated ECM degradation, as ADAMTS-4, MMP3, and MMP13 were downregulated, whilst SOX9, collagen II, and aggrecan were upregulated. Furthermore, TBK1 activates the JAK/STAT signaling pathway. Transfection of cells with the STAT3 overexpression plasmid blocked the beneficial effects of TBK1 silencing. In conclusion, TBK1 is highly expressed in OA. Silencing of TBK1 inhibited ECM degradation.
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