ArticleJournal of advanced research2021
The therapeutic effect of TBK1 in intervertebral disc degeneration via coordinating selective autophagy and autophagic functions.
Article in Journal of advanced research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Epigenetic H3K4me3 activation of miR-155-5p promotes intervertebral disc degeneration via autophagy and ageing in nucleus pulposus cells.Non-coding RNA research · 2026Article
- Restricting intracellularAutophagy · 2026Article
- Article
- Ocifisertib alleviates the gasdermin D-independent pyroptosis of nucleus pulposus cells by targeting GSDME.Scientific reports · 2025Article
- Three-Dimensional Bioprinting for Intervertebral Disc Regeneration.Journal of functional biomaterials · 2025Review
- Lactate and lactylation in intervertebral disc degeneration.Frontiers in molecular biosciences · 2025Review
- Adipose Tissue-Derived Exosome Maintains Metabolic Balance of Extracellular Matrix in Rat Nucleus Pulposus Cells.International journal of nanomedicine · 2025Article
- Mitochondrial quality control: the real dawn of intervertebral disc degeneration?Journal of translational medicine · 2024Review
- Aging and Autophagy: Roles in Musculoskeletal System Injury.Aging and disease · 2024Review
- Apigetrin alleviates intervertebral disk degeneration by regulating nucleus pulposus cell autophagy.JOR spine · 2024Article
- The MnOGels (Basel, Switzerland) · 2024Article
- Omilancor mitigates the senescence of nucleus pulposus cells induced by DDP through targeting MAP2K6.Aging · 2024Article
- Plant-Derived Senotherapeutics for the Prevention and Treatment of Intervertebral Disc Degeneration and Aging.Metabolites · 2024Review
- Mechanism of the Mitogen-Activated Protein Kinases/Mammalian Target of Rapamycin Pathway in the Process of Cartilage Endplate Stem Cell Degeneration Induced by Tension Load.Global spine journal · 2023Article
- Article
- Mitochondrial DNA induces nucleus pulposus cell pyroptosis via the TLR9-NF-κB-NLRP3 axis.Journal of translational medicine · 2023Article
- Cellular Senescence in Intervertebral Disc Aging and Degeneration: Molecular Mechanisms and Potential Therapeutic Opportunities.Biomolecules · 2023Review
- G3BP1 coordinates lysophagy activity to protect against compression-induced cell ferroptosis during intervertebral disc degeneration.Cell proliferation · 2023Article
- TBK1-medicated DRP1 phosphorylation orchestrates mitochondrial dynamics and autophagy activation in osteoarthritis.Acta pharmacologica Sinica · 2023Article
- Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: While its innate immune function has been known, recent works of literature have focused on the role of Tank binding kinase 1 (TBK1) in regulating autophagy and it is unknown whether TBK1 protects against intervertebral disc degeneration (IVDD) through affecting autophagy. Objectives: Here, we aim to explore whether TBK1 is implicated in the pathogenesis of IVDD, and investigated the potential mechanism. Methods: Western blotting and immunohistochemistry were used to detect the TBK1 expression in human and rat NP tissue. After TBK1 overexpression in NP cells with lentivirus transfection, autophagic flux, apoptosis and senescence percentage were assessed. Si-RNA , a utophagy inhibitors and protein phosphatase inhibitors were applied to study the mechanism of autophagy regulation. In vivo study, we further evaluated the therapeutic action of lentivirus-TBK1(Lv-TBK1)injection in a rodent IVDD model. Results: The TBK1 level was reduced in rat and human NP tissue. TBK1 overexpression protected against apoptosis and premature senescence. These functions of TBK1 were abolished by chloroquine-medicated autophagy inhibition.P-TBK1, an activation form of TBK, is involved in selective autophagy through directly phosphorylating P62 at Ser 403, and the activation of TBK1 is also dependent on Parkin manner. TBK1 also activated NPCs autophagy to relieve puncture injury in vivo. Conclusion: We demonstrated that TBK1 overexpression attenuated senescence and apoptosis and promoted NPCs survival via upregulating autophagy. TBK1 represents a promising avenue for IVDD treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.