ArticleActa pharmacologica Sinica2023
TBK1-medicated DRP1 phosphorylation orchestrates mitochondrial dynamics and autophagy activation in osteoarthritis.
Article in Acta pharmacologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- LncRNA Mirt2 Attenuates Osteoarthritis Progression by Promoting miR-429/TBK1-Mediated Autophagy.Immunity, inflammation and disease · 2026Article
- Targeting the SARM1-cADPR-CaArthritis research & therapy · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- The cGAS-STING pathway and mitochondrial metabolism: from mechanistic insights to therapeutic potential in tumor.Journal of translational medicine · 2026Review
- Targeting the mitochondrial metabolite-dynamics-MDVs-MitoEVs axis: a new frontier in osteoarthritis management.Journal of translational medicine · 2026Review
- Mitochondrial-targeted therapy for osteoarthritis: Challenges and opportunities from basic research to clinical translation.Frontiers in immunology · 2026Review
- Gene Therapy for the Treatment of Osteoarthritis: Advances and Prospective.Current pharmaceutical design · 2026Review
- Mitochondrial transplantation for osteoarthritis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Therapeutic potential of IκB kinase epsilon inhibition in preventing meniscal degeneration of early osteoarthritis.Bone & joint research · 2025Article
- Therapeutic restoration of mitochondria-endoplasmic reticulum cross talk for osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DRP1, fission and apoptosis.Cell death discovery · 2025Review
- Dipeptidyl Peptidase 4 (DPP4) Exacerbates Osteoarthritis Progression in an Enzyme-Independent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Harnessing exercise to combat chronic diseases: the role of Drp1-Mediated mitochondrial fission.Frontiers in cell and developmental biology · 2025Review
- Recent development of mitochondrial metabolism and dysfunction in osteoarthritis.Frontiers in pharmacology · 2025Review
- From dysfunction to healing: advances in mitochondrial therapy for Osteoarthritis.Journal of translational medicine · 2024Review
- Mitochondrial transplantation: a promising strategy for treating degenerative joint diseases.Journal of translational medicine · 2024Review
- Protective Effects of Vitamin D on Proteoglycans of Human Articular Chondrocytes through TGF-β1 Signaling.Nutrients · 2024Article
- TBK1 pharmacological inhibition mitigates osteoarthritis through attenuating inflammation and cellular senescence in chondrocytes.Journal of orthopaedic translation · 2024Article
- The role and intervention of mitochondrial metabolism in osteoarthritis.Molecular and cellular biochemistry · 2024Review
- Mitochondria in depression: The dysfunction of mitochondrial energy metabolism and quality control systems.CNS neuroscience & therapeutics · 2024Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dynamics, including mitochondrial fission and fusion, are critical for maintaining mitochondrial functions. Evidence shows that TANK-binding kinase 1 (TBK1) regulates mitochondrial fusion and fission and then mitophagy. Since a previous study demonstrates a strong correlation between mitophagy and osteoarthritis (OA), we herein investigated the potential role of TBK1 in OA process and mitochondrial functions. We demonstrated a strong correlation between TBK1 and OA, evidenced by significantly downregulated expression of TBK1 in cartilage tissue samples of OA patients and in the chondrocytes of aged mice, as well as TNF-α-stimulated phosphorylation of TBK1 in primary mouse chondrocytes. TBK1 overexpression significantly attenuated TNF-α-induced apoptosis and abnormal mitochondrial function in primary mouse chondrocytes. Furthermore, TBK1 overexpression induced remodeling of mitochondrial morphology by directly phosphorylating dynamin-related protein 1 (DRP1) at Ser637, abolishing the fission of DRP1 and preventing its fragmentation function. Moreover, TBK1 recruitment and DRP1 phosphorylation at Ser637 was necessary for engulfing damaged mitochondria by autophagosomal membranes during mitophagy. Moreover, we demonstrated that APMK/ULK1 signaling contributed to TBK1 activation. In OA mouse models established by surgical destabilization of the medial meniscus, intraarticular injection of lentivirus-TBK1 significantly ameliorated cartilage degradation via regulation of autophagy and alleviation of cell apoptosis. In conclusion, our results suggest that the TBK1/DRP1 pathway is involved in OA and pharmacological targeting of the TBK1-DRP1 cascade provides prospective therapeutic benefits for the treatment of OA.
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